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Session III: Invasive Diagnosis and Treatment-6155
Workshop #4- SVT and VT Invasive-Noninvasive Corre ...
Workshop #4- SVT and VT Invasive-Noninvasive Correlation
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Greetings. This is John Miller with Core Concepts in Electrophysiology. I have workshop questions to go over with you. There are about four or five of these. These are my disclosures. You can look at those at your leisure. Here's our first question. A 58-year-old woman undergoes pulmonary vein isolation for treatment of atrial fibrillation. The figure I will show illustrates results of pacing. This is from the ablation catheter and recording from a lasso ring catheter. Both are in the right superior pulmonary vein after pulmonary vein isolation. The best interpretation of these results is that entrance and exit block are present. Neither entrance nor exit block are present. Exit block is present, but not entrance block. Entrance block is present, but not exit block or indeterminate. There are no conclusive findings. Here is the figure. You see you have surface leads, hyst leads, a catheter along the tricuspid anus, the halo, the ablation catheter where stimulation is being performed, and the lasso catheter. Both of those are in the right superior pulmonary vein in a coronary sinus catheter. I'll let you look at this and you can pause. I'm going to go on to the answer. You can rejoin me when you have your choice. The correct answer is that exit block is present, but not entrance block. Why is this? If we look at the figure, we see a couple of things here. We got sinus rhythm going on throughout. These are sinus P waves. It's perfectly regular. Whatever is going on with pacing has no influence on the underlying sinus rhythm. Second, we're pacing at a slightly faster rate. We should be able to see something happening in the sinus baseline atrial rate if we're doing anything to it, but as I said, we don't. When we're pacing from the ablation catheter in the right superior pulmonary vein and recording in the right superior pulmonary vein, we see these signals here. Those are captured PV potentials. Since we're capturing the vein on these four cycles and not getting to the atrium, we have exit block. There's plenty of opportunity to, I mean, this is 350 milliseconds here from stimulus to this P wave. If it's going to exit the atrium, it sure should have been able to, but it didn't. This is a different interval over here. It should have a consistent interval. If it's capturing and connecting, there's no conduction. We have at least exit block. That rules out several of our choices, one of which was that neither are present, one of which is that only entrance block is present, and one of which is it's indeterminate. We're down to just a couple of choices here, just seeing this one finally. All right, what else is going on? There are a couple of other stimuli here. We look here at these intervals along here from the atrial, far-field atrial recording to the pulmonary vein signal that we see here before this next stimulus artifact is fixed at 380 milliseconds. Why would that be? Because it's being conducted. That means we have no entrance block. It is getting into the vein, but we have exit block. So we have conducted PV potentials from atrium to the PV, showing lack of entrance block, and these now light blue arrows show stimulus artifacts that are not followed by captured PV potentials because the PV sleeve is refractory. It's just fired here. It's refracted. It's not lapsed by this time. So what we have is a capture of PV potentials when it's possible that are not conducted out. That is exit block, and we have PV potentials that are conducted into from the atrium. Now, if you're a patient and you have atrial fibrillation that's coming from the veins, would you rather have entrance block or would you rather have exit block? I'd rather have exit block. Now, usually these track together. So if one has entrance block into a vein and you have bonafide entrance block, PV potentials are gone. You can't see them at all in areas where you should have been able to see them with electrodes in the vein. That usually correlates probably 95, 98% of the time with exit block also. There's some of us who check for exit block whenever possible because what I want my patients to have is stuff not getting out of the pulmonary vein. I don't care if it can get in, really. I just care if it can't get out. So I check for exit block. Here's a situation in which we fortunately have exit block but not entrance block. Question number two, also about pulmonary vein isolation. A 63-year-old woman undergoes pulmonary vein isolation for treatment of symptomatic atrial fibrillation. After completion of antral PV isolation, adenosine is injected rapidly. The ablation catheter is pacing constantly from the left superior pulmonary vein, and the lasso catheter is in the right superior pulmonary vein. The figure demonstrates which of the following, entrance block to the left superior pulmonary vein, exit block from the right superior pulmonary vein, entrance block to the right superior pulmonary vein, conduction from right superior PV to left superior PV, or conduction from left superior PV to atrium to right superior PV. Okay, here's the figure. So at this point, we're pacing along consistently in the left superior pulmonary vein. We're recording with a separate catheter in the right superior pulmonary vein. That's where the lasso is here. And adenosine is being injected up here. All right, I'm going to pause. You can pause and mull this over a little bit and then come back when you have your answer. The answer is, conduction from left superior pulmonary vein to atrium to right superior pulmonary vein. All right, why is this? We're only pacing in the left superior pulmonary vein. It's being done consistently. It's not seeming to capture anything over here. But the effect of adenosine after a few cycles, and typically a little before its most profound effect on the AV node, is to improve the decreased arresting membrane potential of the atrial muscle cells outside of the pulmonary vein, injured such that they're partially depolarized and can't give a regenerative action potential with regular stimulation. But when you gear up their adenosine-sensitive potassium channels, now they can repolarize. So now they're able to conduct just for a few cycles here. So it's clear that we have now capture of the left superior pulmonary vein because that's the only thing we're pacing. And we have atrial recordings here in the his bundle recording and in the coronary sinus that are at paced cycling. So we're getting out of the left superior pulmonary vein to the atrium. Meanwhile, we're recording signals over here in the right superior pulmonary vein. They're not occurring spontaneously either before or after. So it seems as though they're being conducted to from the left superior pulmonary vein to the atrium, and then into this vein because these are occurring after the... There's some far field signals that we see here that are just atrial signals. And then these are the PV signals along in here from the right superior pulmonary vein. So the correct answer is that we're capturing the left superior pulmonary vein, conducting to the atrium, getting out of the left upper vein and getting into the right superior pulmonary vein. So that was our choice conduction from left superior PV to atrium to right superior pulmonary vein. D is not correct because we're going from left to right, not going from right to left. We don't have entrance blocked to the right superior. We got into the right superior. That's how we got those lasso recordings. We don't have exit blocked from the right superior. We're not stimulating there and it's being conducted into, not out of, and we don't have entrance blocked to the left superior. We're getting out of the left superior. All right. So there's that. Question number three, a 58-year-old man underwent catheter ablation of persistent atrial fibrillation two years ago. There's a theme here and returns for evaluation of recurring palpitations. The last four stimuli of overdrive pacing during a tachycardia that has been induced are shown followed by resumption of the same tachycardia. The site of pacing is best characterized as inner loop, outer loop, central isthmus, adjacent bystander, remote bystander, or the data are inconclusive. Here is the figure. This is overdrive pacing from the ablation catheter as indicated with the S's during a tachycardia that started way off on the left side of the screen, overdrive pacing during tachycardia, and now we have a resumption of the same tachycardia. I'll pause at that for you. And speaking of pause, you can pause the presentation now, contemplate your ideas and come back when you have your choices. The correct answer is this is an adjacent bystander. Adjacent bystanders, in my experience, are relatively rare in the atrium. They're not so rare in the ventricle, but they're relatively rare in the atrium. I'm not sure why that should be, but it is. Obviously, it has something to do with the architecture of the scar and how many side channels you can have. The features of these different sites are shown in this table here, the different choices that were presented in the distractors. The timing of the signal in an air loop and an outer loop is systolic. So let's think of it in another way. If you're in the mid-diastolic quarter, obviously that's mid-diastolic. The rest of the cycle has to be completed somewhere. So if you're in the middle of diastole here and you're going exit and you're going around to get back to the entrance, this area where you're going back around, if it's a tissue that's outside of scar, it would be an outer loop. And when you pace there, you get some pacing that looks like the muscle is being captured elsewhere. It doesn't look exactly like tachycardia because there's some tissue that's outside the circuit. It's a fusion situation. An inner loop is down on the inside here, completely bounded by a scarf. So you've got a diastolic quarter. And then during systole, when the signal is returning, it's in this inner loop. And when you pace from there, it has nowhere else to go. There's no fusion. So it looks exactly like tachycardia as it goes out the exit. So both of those are systolic recordings. And as I said, in the situation with the outer loop, you're capturing some additional tissue that is not directly inside the circuit. In most cases, you're capturing some additional tissue. So it will look like there is fusion. So fusion is present in outer loop. Since the inner loop is bounded by a scar, there won't be any fusion. Post-pacing interval minus tachycardia cycle length will look like it's in the circuit because it is in the circuit. Both of these are in the circuit. And the stimulus to pick a reference atrial electrogram, in the case of atrial erythema, the stimulus to reference minus the electrogram reference is also quite close, indicating that, again, you're not very far off the path. Central isthmus we're all familiar with. This is a diastolic recording. And fusion is absent because when we pace there, it has to go out the exit for the tachycardia to be actually entrained. PPI minus TCL within bounds that we're all familiar with. And the stimulus to your reference atrial electrogram minus the electrogram during tachycardia to that same reference is quite close as well. Remote bystander can have any kind of timing, really. It probably isn't going to be diastolic, but it can be early systole, mid systole, late systole. But technically, it could be anything. Fusion is always going to be present and is always going to have a long PPI minus TCL and a long stimulus to reference minus electrogram during tachycardia to reference because it's outside the circuit. It's basically anywhere else in the atrium. You have a left atrial circuit, you're pacing in the right atrium, and it entrains the tachycardia. You've got a remote bystander. Inconclusive would be when any of these other, it could be a combination of any of these things. PPI minus TCL is short, shorter than zero. That's this leapfrogging business where you're capturing more tissue than you think, and you think you're pacing from here and sending it forward, but you're actually capturing a much larger area. Instead of stimulating here, you're actually stimulating, capturing tissue there and sending it forward in the loop. The one I didn't cover just yet is the adjacent bystander. This has a juicy looking electrogram. It's a nice diastolic electrogram, usually early, mid diastolic. When you pace from there, fusion is absent, just like a mid diastolic recording. The key is that PPI minus TCL is in excess of 30 milliseconds, so it's not on the main highway. The stimulus to reference minus the electrogram bearing tachycardia to reference is long as well. This is because it has to... Your main corridor, your main circuit is like this, going around like this. You've got this spur off up here. If you're pacing from there, it has to propagate into the main traffic, go around once, come back to that spot, and then go back up into this little bystander corridor there. PPI minus TCL is long. The stimulus to electrogram... Stimulus to reference is different from the electrogram to reference. What do we have on our recording through that? Well, we have a signal that is in diastole here, late diastole. That's our electrogram during tachycardia. It's between P-waves. Yellow is diastole here. When we compare the pace sequence, I just copied one of these and superimposed it over here. It's a pretty doggone good match to the tachycardia. There is no fusion. It is one of these guys here. Fusion is absent. Absent. Absent. Okay. One of those guys. Interloop. Entrance, exit. Main corridor or interjection bystander. It's one of those. We know it's not interloop because this has diastolic timing, not systolic timing. It's not an entrance site because the timing of the electrogram is not in the early portion of diastole. It's in the mid to even late portion of the diastole. It could be either the central instruments or the adjacent bystander according to this. So far, so good. There it is down to two. The trick here is then the electrogram to reference is 90 milliseconds during tachycardia, but the stem to that same reference electrogram, this guy up here, so from here, this electrogram to there, this dashed line, 90 milliseconds from the stimulus that captures that electrogram to that same reference, 145. The last I checked, that's in excess of 30 milliseconds. My math isn't so great these days, but I'm pretty sure that's more than 30 milliseconds. So that's wrong. The PPI is longer than the tachycardia cycling by the same amount. This is a 55 millisecond difference. This is a 55 millisecond difference. This is the hallmark. These are the hallmarks of an adjacent bystander. Again, an unusual visitor in our atrial tachycardias. These are the cardinal features in. There's concealed fusion. You don't see any evidence of fusion. There has to be some antedromic propagation in the circuit somewhere. We just don't see it with the electrodes that we have. There's no evident fusion. PPI greater than tachycardia cycling in excess of 30 milliseconds usually. It's well in excess of it. I've seen as much as 100 milliseconds difference. Stem to reference, this reference electrogram that we're picking here is in excess, a significant excess of the electrogram during tachycardia to reference electrogram. That's the adjacent bystander. Question number 4. A 44-year-old man has recurrent atrial arrhythmias following RF catheter ablation, that is, pulmonary vein isolation, roof, and mitral isthmus lines for treatment of atrial fibrillation. The recordings in the figure I will show illustrate entrainment of a right atrial circuit, entrainment of a left atrial circuit, overdrive pacing during a focal right atrial tachycardia, overdrive pacing during a focal left atrial tachycardia, or no diagnostic findings. Here are the recordings. You can ponder that for as long as you wish. Rejoin us with your answer. I'm going to go ahead with my answer because I know what the answer is. It happens to be no diagnostic findings. Why is that? Well, we're overdrive pacing during a tachycardia, are we not? Yes, we're delivering a stimuli during a tachycardia. We should say we started with this tachycardia, we're doing overdrive pacing during it, and we end up with the same tachycardia. A piece that I didn't say in there is we have accelerated all electrograms to the pace cycle length because we haven't. If you look carefully here, look at this electrogram here in Halo 13-14. You don't see it here. You see it here. You see it earlier than the stimulus artifact here and still earlier here. We weren't controlling the Halo electrodes at all. Maybe we're controlling some tissue somewhere, but I can't interpret this. I can't tell you what the post-pacing animal is here. Certainly, if we're stimulating from this electrode, or one adjacent to it, we really should be capturing tissue pretty close by, don't you think? This is not capture. Any inference you make from any measurement you make, good luck. You might, by chance, be right. You might stumble on something, but it's only because you followed the ancient rule, a blind squirrel can still find a nut. There's a lot of nuts out there. What we have here is stimulation during tachycardia, but it's not effective stimulation because it never captured. Now, another question that might be asked in a situation like this on an examination was, what do you need to do to fix this? Do you need higher output? I don't think so because the tissue that we're stimulating is refractory here, right? There's no amount of output that you can get to do this. Do you need to pace faster? Well, maybe. That's not the problem. The problem is you're not capturing. Maybe you've got adequate output here. Maybe you need to pace for longer. So it's just coincident with the electrogram here. Maybe if you pace for a couple more cycles, you'd actually catch up. You shouldn't stop pacing just because you captured a couple of local electrograms. Should you wait until all the relevant electrograms are accelerated to pace cycle length? But this is a situation where it's tempting to measure a post-pacing interval and say, hey, I know something. I know what's going on here, and you don't know nothing. It's as though you didn't even pace here. And you should just put a, do not look at this on your log. Of course, that makes people look at it. That's just human nature. But don't make any inferences off this. Okay, so here is the important information here. You look at where we were stimulating, and you see, you know, we didn't ever affect any of these electrograms that are right on top of where we were stimulating. The pace cycle length is 350. Tachycardia cycle length is 370, 375, 380. I don't know why it's a little bit shorter over here, but we certainly didn't control any, we certainly didn't accelerate all the electrograms at the pace cycle length. This last one, maybe we did capture it. So you could say, okay, I put in a single extra stimulus. The rest of these don't count. Okay, maybe that makes some sense there. But I'd be a little bit wary of making inferences on just one. And especially in light of this, because this cycle here is spontaneously occurring at an interval that's less than this. So you can't even say that, well, at least we brought one of these in with our last extra stimulus. You can't tell that because we got a shorter cycle over here that wasn't stimulated. So do it right. Go big or go home. No clear capture, no interpretation. Question number five. The lasso as labeled here, the ring catheter, in this case is in the left superior pulmonary vein, placed there after pulmonary vein isolation. All pulmonary veins we think have been isolated. We're gonna be stimulating from that catheter in the left superior pulmonary vein. This figure shows PV capture with conduction to atrium, PV capture without conduction to atrium, no PV capture, but no influence on atrium, or unclear PV capture, but no influence on atrium. And you can think about that and make some measurements and think about some stuff and come back when you're ready with your answer. I'm ready with mine. The answer is PV capture without conduction to atrium. How do we know that? I've shown you enough information here to get the correct answer. I've shown you that we have sinus rhythm coming along here on its own, and that we have isolated firing in a pulmonary vein. There's no relationship between this potential and what preceded it or what follows it. So it's entrance block and exit block of these spontaneous impulses, okay? And these are quite regular here. That's a key element here. They're so regular that you would expect to see the next one here, and you would expect to see the next one after that right here. You don't. Why don't you see them? Because they've been captured by the stimulation in that vein from the ring catheter, okay? We have PV capture. It's either A or B. Now, does it have an influence on the atrium? Well, then you look at what happens on the surface. You can see the stimulus to P wave. And one thing that I tell my trainees is don't get hung up looking, trying to see is this interval different from this interval? Well, if the sinus rate is the same throughout and the stimulation rate is the same throughout, then what happens here is gonna be minimally different from here maybe, but greatly different from over here on this side. And it's easy to see that this stimulus to P is significantly longer than that stimulus to P there. So if we measure those guys, you can see that quite evidently there. And so there is no influence of the stimulation on the sinus rate. It could be in a different person as far as that goes. This is an isolated vein, entrance and exit block. We have PV capture inferred by the absence of recordings of PV potentials when they should be there if we weren't capturing them. So their disappearance means that we were capturing them and we're not conducting to the atrium. I thank you for your attention. Hi, this is Frank Marchlinsky. I'm glad to be part of the core concepts curriculum and thank the organizers for inviting me. This is my questions for workshop four to get everybody oriented. I'm from the University of Pennsylvania, by the way. Here are my disclosures. Okay, so this is in the order of the cases, case 12. And this slide shows several images, a couple of images recorded at the time of a pulmonary vein isolation procedure and two tracings that were recorded. And we'll go back to those tracings and images in a second. But I just want to read to you the question that's going to be asked. So these are patients with multipolar catheters as shown in the fluoroscopic image and we'll get back to it in a second. And one catheters position also in the right superior pulmonary vein after a lesion set around the antrum during pacing from the two multipolar catheters. One is in the coronary sinus and the second in the right atrium extending into the superior vena cava. So you do not see the coronary sinus catheter recordings but you will see the recordings from the high right atrium and the recording from the pulmonary vein. And there is a series of options for the statements that are most likely, the statement that's most likely to be true related to the images in the figures 12.1 to 12.4. And the choices will be pacing from additional left atrial sites is required to determine if conduction is still present into the right superior pulmonary vein, the signals on the multipolar catheter in the right superior pulmonary vein shown in tracing 12.3 represent four field signals from the SVC. The pulmonary vein demonstrates entrance of conduction into the vein with CS but not SVC pacing and additional ablation is required and DPV entrance block and exit block are demonstrated during the pacing maneuvers. So here, those are the choices. Let's go back to the images. So again, this is the multipolar catheters, one in the CS, one extending up into the superior vena cava and then the catheter, multipolar catheter in the position in the right superior pulmonary vein. This is the tracing recorded from the right superior pulmonary vein during CS pacing. And this is from the recordings from the superior SVC and right atrium on the middle tracing 12.3 and 12.4 shows the tracings with SVC pacing. So here's the right superior pulmonary vein recordings and then the SVC and RA. So rather complicated, I hope you can both see the question and also see the images, it will make it easier but we'll have to work through without that for the moment. And again, here's the choices. And let's see if you can pick the correct answer. Okay. Okay, here's the information now with the figures highlighted. And what we see first of all are with CS pacing, the presence of these low amplitude signals. And of course the question is, do they represent vein signals or far field signals that time with the superior vena cava? And so that's what we see with tracing 12.3 and 12.3 can't be sure whether these truly represent vein signals. Suffice it to say they're not very late if they're vein signals and they do time with the distal catheter, multipolar catheter that's positioned up into the SVC. And then with SVC pacing, all of these signals are immediately pulled in suggesting that indeed these signals represent far field identification of recordings from far field from the superior vena cava. They're all moved in with SVC pacing and they don't represent pulmonary vein signals. So there's no evidence of conduction into or out of the vein. So the answer, correct answer is the signals on the multipolar catheter in the right superior pulmonary vein shown in 12.3 represent far field signals from the SVC. And by pacing the SVC, we pull the far field signals in on the multipolar catheter in the right superior pulmonary vein. And that's consistent with them indeed being just a far field signals. Okay, the other answers of course are no. There's all those small potentials that may represent pulmonary vein signals. They're not delayed. And the time with SVC signals, and again with SVC signals, they're pacing, they're pulled in, et cetera. Okay, let's move on to the next case. So here's case 13, the 74 year old man with symptomatic atrial tachycardia prior surgical mitral valve repair and LA appendage ligation. And the patient obviously presents with this tracing in the atrial tachycardia in response to pacing. And pacing is performed in this case from the distal and proximal coronary sinus during the tachycardia. And stimulation is being performed in tracing 13.4 from the left atrial appendage region while recording from the left atrial septal region during ablation and with termination of the tachycardia. So this is termination of the tachycardia. This is pacing from the left atrial appendage. This is the recording from the septal side of the ablation line as it's being performed. So here's the question. Based on the tracings 13.1 through 13.4, which of the following is most likely to be true? Right atrial incisional atrial tachycardia from prior surgery is present, has been successfully ablated. Ablation of LA roof dependent flutter has been successfully performed. Mitral annular flutter is present and has been successfully ablated. Or D, although the arrhythmia has terminated with ablation, block in the ablation line has not been established. Okay. I believe that most of you probably gave the correct answer. We gave enough clues from the tracings that we're dealing with mitral annular flutter, ablating in the upper part of the septum, terminates the tachycardia, and shows evidence of endocardial left atrial block with long interval on the opposite side of the area where that was targeted for ablation. So, here is evidence consistent with mitral annular flutter, one of the tracings 13.2 and 13.3, showing distal and proximal CS spacing with a post-pacing interval approximating the tachycardia cyclin, consistent with a mitral annular flutter. In this case, rotating in a counterclockwise direction. And then, this is the site of the ablation catheter recording at the time of the tachycardia termination. And then, subsequent pacing as shown in tracing 13.4, in the original figure, from the left atrial appendage region, documented that the last area to get activated in the left atrium was the recording just adjacent to the ablation line that targeted this antraceptal region, and it was very late, consistent with termination of this mitral annular flutter from the previous tracing, and now demonstration of endocardial block and successful ablation of the mitral annular flutter. Okay. Our next case, case 14, multipolar recordings from the right superior pulmonary vein, coronary sinus, and superior vena cava, right atrium, that's referred to as the crista catheter that extends into the superior vena cava, and the bottom of the LA after pulmonary vein isolation. So, this is recorded from the bottom of the LA, coronary sinus catheter extending into the superior vena cava, and then the catheter in the right superior pulmonary vein. These are the recordings, and then your interpretation of this tracing 14.1. Which of the following is most likely to be true? The right superior vein has been transiently reconnected with adenosine, and that's what's being shown on the tracing. B, the right superior pulmonary vein is isolated as evidenced by isolated PV firing. C, there is evidence of right superior pulmonary vein entrance block, but not exit block. And D, APDs from the superior vena cava are activating the right superior pulmonary vein. Okay, the correct answer is C. There is evidence of right superior pulmonary vein entrance block, but not exit block. Let's go over the answer in a little bit more detail by looking at the figure again. In this figure, we have two electrogram displays from the right superior pulmonary vein where we see isolated firing. That isolated firing, however, does importantly appear to conduct out of the vein. So, there's no evidence that we're entering the vein, but we are exiting the vein that fires in an isolated fashion. So, entrance block still present, exit block not present, conducting out of the vein. This is not a typical response to adenosine. There's no slowing of the rate of the arrhythmia, PR prolongation. So, there's no suggestion that you've given adenosine. Might you see an improvement of conduction and return of conduction out of the vein with adenosine? Yes, but there's no other associated clues. So, the best response would not be the adenosine response. And clearly, there is isolated firing, but the vein is not isolated. So, even though there's entrance block, the vein is not isolated based on presence of exit out of the vein. And there's no evidence that the APD is originating from the SVC. They're actually, as you can tell, originate from the earliest activation is from the pulmonary vein itself. So, the isolated firing is from the pulmonary vein, not an APD from the superior vena cava. So, the best answer is, again, see an evidence of entrance block, but not exit block. Here's the pacing from this vein, and just showing with conviction that we captured the vein sleeve and then conducted out of the vein, albeit with some delay, showing additional evidence that there's no exit block from the vein, but there was entrance block. Pacing is performed during this wide complex tachycardia from the mapping ablation catheter. And based on this tracing, you see the wide complex tachycardia, and then pacing that starts during the tachycardia and continues to the right of the screen. What best describes the observations on this slide? A, the site of stimulation and recording is an entrance site to the VT isthmus. B, ablation at this site is likely to terminate ventricular tachycardia. C, VT stops and restarts, suggesting an automatic mechanism. And D, the observations noted on the tracing are consistent with bundle branch re-entrant VT. Okay, so let's go through each one of these answers. So, A, it's not an entrance site. There's activation response to pacing is consistent with an isthmus site. The activation with pacing mimics that of the VT. We tend to see a complete change in the morphology when we're pacing from an entrance on the opposite side of the isthmus. And this stim-to-electrogram interval, to QRS interval, although long, is not extremely long, consistent with something either from a distal isthmus or from an early entrance, exit site. Exit site. And so, that makes A incorrect. Ablation at this site is likely to terminate VT. The answer to this would be yes. This is an extra, a first beat of pacing that actually is a non-propagated stimulus that terminates the tachycardia. And we have, with continuation of the pacing, a long stim-to-QRS complex, consistent, as I said, with a perhaps an latter isthmus site or early exit site, something that might be anticipated with ablating in this area, based on the two observations, to have a higher likelihood of terminating the ventricular tachycardia. So, a non-propagated stimulus and a long stim-to-QRS interval with the pacing mimicking the ventricular tachycardia. Again, this is paced complex and not reinitiated VT. We have the pacing at 360 in that QRS complex, clearly being that matching that interval at 360. So, it's paced. Okay, this is case 16 of workshop 4. On the top, we have tracing 16-1 showing three ventricular tachycardia morphologies. In the bottom, we have the baseline 12-lead ECG QRS complex. And here's the question. I also have the tracings in the lower right, so you can look at them as we read through the question. This is a 32-year-old woman with three monomorphic VTs and the ECG recording in sinus rhythm, as shown. The transthoracic echo and MR shows a little bit of RV dilatation, but no segmental wall motion abnormalities and no late gadolinium enhancement. No abnormalities are identified on genetic screening. Which of the following statements is true from the list below? The patient demonstrates a major task force criterion for the diagnosis of ARVCM based on the inverted T waves in the precordial leads in sinus rhythm. B, sinus rhythm ECG changes in V1 and V2 suggest the diagnosis of Bergada syndrome. C, the patient is likely to demonstrate electrogram voltage abnormalities on the epicardium of the RV outflow tract. And D, the patient has several morphologies of idiopathic RV outflow tract VT, which will typically respond to treatment with beta blockers. OK, let's look at our answers. The patient demonstrates inverted T waves, but they're inverted in V1 and V2, and this is a minor criterion. We'll show you the task force criteria for ARVC in a second. She had three minor criteria present or a borderline diagnosis of ARVC based on task force criteria alone. The sinus rhythm ECG changes in V1 and V2 don't suggest the diagnosis of Brigotta syndrome. We'll show you an example of that in a second. And then it is true that the patient is likely to demonstrate electrogram voltage abnormalities on the epicardium of the RV outflow tract. Multiple VT morphologies are identified. All of them have poor R wave progression consistent with a free wall origin. An epicardial origin is suggested with the delayed QRS upstroke in a traumatic QS complex in V2. And the recognition that ARVC is frequently a process that involves more involvement in the epicardium than the endocardium. This is not typical ECG morphologies associated with idiopathic RV outflow tract tachycardias. It's unusual to have sustained monomorphic VTs with multiple morphologies. And there's a variable response to beta blockers even if that were the case. So answer D would be inappropriate. The best answer is C. This slide just shows the task force criteria for the diagnosis of ARVC. Some of them based on global and regional dysfunction in terms of RV size and contractility. Patient had some increase in size, but no other imaging criteria consistent with the diagnosis. She did not undergo a biopsy. Here are the repolarization abnormalities, depolarization abnormalities, arrhythmia, manifestations, and genetic abnormalities consistent with task force criteria. And the patient had inverted T waves in V1 and V2, which suggests that it might be abnormal, but it doesn't go beyond V2. So it's a minor criteria. She also has evidence of an inferior axis QRS morphology. In this case, although the task force criteria were not met for the definitive diagnosis, it is unequivocal based on the morphology of the QRS complex during the ventricular tachycardia is that this is likely an epicardial source for the arrhythmia. And indeed, in this patient, the endocardial voltage map was minimally abnormal. The epicardial voltage map showed an extensive area of low voltage. Each of the black dots highlighting abnormal, dramatically abnormal, electrograms consistent with an epicardial substrate that was targeted successfully for ablation. Here's ECG demonstration of Brugada syndrome V1 and V2 ST segment elevation that was not present in this patient. This is a typical pattern with the characteristic depolarization abnormality on the outflow tract region with fragmented electrograms that can be targeted for effective substrate ablation. These patients typically do not have monomorphic VT. They have polymorphic VT. And some additional references for you to take a gander at in your spare time. This is Bill Miles. I'm professor of medicine at University of Florida. And I've been asked to give another workshop, mainly on the SVT ablation modules that I gave earlier. We're going to do this a little bit like I did workshop 3. And that is, I'm going to show the question and the alternative answers. I'm going to show them the electrograms. I'm going to flip back and forth a little bit because, unfortunately, they're not on the same slide. And we only have one screen to present with. And then I'm going to ask you to, if you want to study the electrograms and study the answers, pause your tape. And I'm going to pause for five or six seconds and then keep going. So you can either cheat and just go with me, or you can stop the tape with each one and study the electrograms a little more carefully. These are my disclosures. We'll start with case 1. You are applying the first radiofrequency energy delivery in a patient with slow, slow AV node reentry. The ablation catheter is located in the lower third of the septum between the tricuspid annulus and the os of the coronary sinus. Which of the following are true? So I'm going to show you the electrograms in a minute. You should not terminate RF delivery. This site is not an appropriate RF ablation site for the right inferior extension. The patient does not have a right inferior extension. The patient may not have a retrograde fast AV nodal pathway, or the AV node reentry ablation procedure should be abandoned due to a very high risk of AV block. And here are the tracings. The patient wiggled a little bit, so the surface electrograms are a little bit crummy. But the catheter electrograms are good. We have the right atrium. We have his leads. We have ablation catheter. We have coronary catheter from proximal to distal, and we have a right ventricular catheter. So we start delivering radiofrequency somewhere around here. I didn't mark exactly where it was. And what do you do? You should not terminate RF delivery. The site is not an appropriate RF site for the right inferior extension. The patient does not have a right inferior extension. The patient may not have a retrograde fast AV nodal pathway, or you should abandon the case due to the high risk of AV block. Here are the electrograms again. So I think on your tape, you can go back and forth. And I'm going to pause for a few seconds, and then I'm going to keep going. So let's look at what I think is the answer. I think the answer is this patient may not have a retrograde fast AV nodal pathway. You can see here that the patient has junctional extrasystoles that don't even interrupt sinus rhythm. So you have junctional extrasystoles. The junctional extrasystoles don't go to the atrium, and you have continuation of sinus rhythm. So since this is the first energy delivery, you should terminate immediately and make sure you know where you are and that AV conduction is OK. However, it is the appropriate site for the right inferior extension. It may be that this patient has a tachycardia that involves the right inferior extension, maybe the left inferior extension, but there is no retrograde fast pathway in this patient. So when you stimulate the right inferior extension with thermal energy from the RF, you get junctionals, but they can't get out the retrograde fast. So that's what I think is going on here. You don't want to just stop, but you do have to be cautious when this happens. So if this is the first RF delivery, the RF should be terminated to make sure antergrade AV nodal conduction is intact. However, rather than this phenomenon indicating damage to the fast pathway, it may indicate that there is no retrograde fast pathway conduction in this patient who has atypical AV node reentry. If there is no retrograde fast pathway, heat-induced automaticity of the right inferior extension will not conduct to the atria, but can still potentially eliminate the AV node reentry. Once you're convinced that this is the case, several short energy deliveries can be given to complete the ablation, watching carefully for any evidence of AV conduction slowing. Other alternatives are to try to overdrive, pace the atrium during energy delivery, attempting to wake up the retrograde fast pathway with adrenergic stimulation, or possibly switching over to cryoablation. So this is the same patient. You can tell that during ventricular pacing, even at slow rates, he had no evidence of a retrograde fast pathway. VA is long, and earliest activation is in the proximal CS. And during tachycardia, the VA is longer than it usually is in typical slow fast AV node reentry, and earliest activation is in the proximal CS. So this is preablation diagnostic electrophysiology that gives us a clue, even before that ablation, that there may be either no or a very poor retrograde fast pathway, and helps do the ablation safely, having this knowledge. And you can tell that when we stopped ablating, those junctional stopped, and AV conduction was intact. This is a different patient. These junctional exocystoles are the good ones. They normally occur upon heating of the right inferior extension. The VA conduction during these junctional exocystoles is presumably via the retrograde fast pathway. It indicates no impending damage. And if VA conduction blocks during RF delivery, or if the exocystoles become rapid, ablation should be terminated. So this is a different patient than what I showed you with the question. This was a patient with typical slow fast AV node reentry. And these good junctionals often slow out gradually during the ablation. And then you can see that AV conduction is normal, even though we're continuing to give ablation. All right, let's go to the next case. This rhythm occurred spontaneously post AV node reentry ablation during high dose isoproteinol infusion. An atrial extra stimulus is introduced from near the coronary sinus ostium. Which of the following is true? The ablation was successful. The tachycardia is most consistent with non-reentrant junctional tachycardia due to isoproteranol. The tachycardia is an atrial tachycardia due to isoproteranol. AV node reentry is gone, but there is an accessory pathway present. Or E, decremental conduction is confirmed in a slow pathway. So let's look at the electrograms. Here are the electrograms. We have five surface leads, a right atrial lead, four his bundle leads, coronary sinus from proximal to distal, and then the right ventricle. And I gave you some measurements on this one. OK, so I'm going to go back for a second. The choices are the ablation was successful. The tachycardia is most consistent with non-reentrant junctional tachycardia due to isoproteranol. The tachycardia is an atrial tachycardia due to isoproteranol. AV node reentry is gone, but there's an accessory pathway present. Or decremental conduction is confirmed in a slow pathway. Here are the electrograms. And all right, so if you want to study them further, pause the tape. I'm going to pause for a few seconds, and then we'll go for the answers. All right, so let's look at the answer. I think the answer is decremental conduction is confirmed in a slow pathway. The ablation, therefore, is not successful, and it's not a non-reentrant junctional tachycardia, and it's not an atrial tachycardia. So an atrial extrastimulus is introduced from the region of the coronary sinus ostium about the time that HIS is activated, or a little bit before. It has no effect on the immediate QRS or HIS, but delays the subsequent QRS. This suggests it collided with retrograde activation, coming up the fast pathway, but entered an anagrade slow pathway, resulting in delay of the AV node reentry. Therefore, the ablation was not yet successful. Now, this maneuver can either result in a longer VV interval or a longer HH interval. They're the same. It can advance the VV interval, or it can totally block in the slow pathway and terminate tachycardia. If it were an ectopic or a non-reentrant junctional tachycardia, you'd have to get even earlier, and it would be this V that would be advanced. So this patient needs more ablation. The fixed VA interval after the PAC, the fact that the A seems to be joined to the V, makes atrial tachycardia an unlikely diagnosis. And here's just an earlier PAC that, as I mentioned before, also is diagnostic, as long as this isn't a serendipitous termination of tachycardia. This early PAC that did not advance this V, but terminated tachycardia, also confirms that the tachycardia is AV node reentry. All right, next case. A 24-year-old male with no evidence of structural heart disease is referred for recurrent wide QRS tachycardia. Ablation for this tachycardia should be aimed at the rightward inferior extension of the AV node, or the slow pathway, the right bundle branch, the lateral tricuspid annulus, the site of earliest ventricular activation during tachycardia, or the site of earliest atrial activation during tachycardia. And I'm going to show you two slides on this patient. Here's a slide of his tachycardia. We have five surface leads. We have a right atrial lead. We have proximal and distal hiss. And we have proximal to distal coronary sinus. And we have a right ventricular electrogram. All right, so that's the tachycardia. The next slide shows a halo catheter on the tricuspid annulus and a coronary sinus catheter in the coronary sinus during sinus rhythm and during that same tachycardia that we showed you on the last slide. So let's go back, look at the choices, and then we'll look at the electrograms. Ablation should be aimed at a rightward inferior extension of the AV node, the right bundle branch, the lateral tricuspid annulus, the site of earliest ventricular activation during tachycardia, or the site of earliest atrial activation during tachycardia. Here's the tachycardia. I've labeled the H. It didn't come out of the stimulator with those Hs labeled, but I thought that might be helpful. And here's sinus rhythm and tachycardia with catheters along the tricuspid annulus and the mitral annulus. All right, so pause the tape, study the choices, and study the slides. I'll pause for a few seconds, and then we'll go forward. All right, so here, this is a young person with no structural heart disease, so this probably isn't Here, this is a young person with no structural heart disease, so this probably isn't bundle branch reentry, and we're going to make an argument that it's not AV node reentry, and we're going to talk about whether to ablate the lateral tricuspid annulus, the earliest ventricular activation, or the earliest atrial activation. This is antidromic AV reentry utilizing an atrial fascicular pathway, and in this particular case, we go down an atrial fascicular pathway or basically an accessory, a right lateral accessory AV node that inserts into the moderator band right bundle distally, activates the apex of the ventricle. Remember, an AV connection should activate the base before the apex, but this right ventricular apical lead is very early, so the apex is being activated, and at the same time, at the beginning of the QRS, the hiss is being activated, and it's being activated in a distal, whoops, a distal to proximal orientation, and then retrograde conduction goes up the hiss through the node, and the atrium is activated concentrically, so this is antidromic AV reentry utilizing an atrial fascicular accessory pathway. Where should we ablate this? Well, it's an accessory AV node and hiss over on the right lateral wall, so if you put a halo catheter around the tricuspid annulus, you might be able to record a potential on the right lateral wall, right lateral annulus, I guess I should say, that is separate from the hiss potential and during tachycardia precedes the QRS, so you go up the, you go up the path, I'm sorry, you go up the node, activate the atrium, cross over to the right lateral area, go through the little accessory AV node, the residual AV node or the atrial fascicular, you record a fascicular potential from the atrial fascicular, and then you activate the atrium, so the best target is this, it's that fascicular potential on the, on the lateral wall. This is antidromic AV reentry utilizing an atrial fascicular pathway as the antigrade limb, and the right bundle hiss and AV node is a retrograde limb. It represents an accessory AV node hysperkinesis system traversing the right free wall and a sharp potential analogous to a hiss potential in that region is the best ablation target. Attempts to target the distal ablation site are more difficult and may result in a right bundle branch block, and a right bundle branch block may prolong the tachycardia circuit, it'll now go over and go up the left bundle branch, and it may make the tachycardia more incessant, so the first place to look to ablate is to look for fascicle potentials on the tricuspid annulus laterally, and that's where you want to ablate. You also don't want to ablate at the earliest atrial site because you're coming up the AV node, and if you ablate at the earliest atrial site, you may get AV block, so you don't ablate at the earliest atrial site, you don't ablate at the earliest ventricular site for the reasons that I gave. You would try to find this fascicular potential on the tricuspid annulus and ablate there. 10 to 15 percent of atrial ventriculars are of Maheim-like tachycardias are not from atriofascicular, but they're from atrioventricular, but they have the decremental unidirectional conduction properties of Maheim fibers or atriofasciculars. They behave like atrioventriculars, but they look almost like the Maheim tachycardia in the last tracing, except that the ventricle is late, the RV apex is now not early, the hiss is buried somewhere in this V, it's not at the beginning of the QRS, and if you look around, you can find a ventricular potential somewhere along the right lateral wall that precedes the QRS enough that you can ablate in that site and get rid of it. So about 10 or 15 percent of Maheim tachycardias are not actually atriofascicular, but they're atrioventricular, and the ablation technique is a little bit different. Here's that patient that I showed on the previous slide that we ablated at that early ventricular site, and after a few seconds we get antergrade accessory pathway block. Very good. Let's do another case. Adenosine is given a few minutes after cryoablation of an epicardial postreceptal accessory pathway from the middle cardiac vein. The atria are paced at a constant cycle length of 800 milliseconds. Why does the QRS widen? Adenosine, is it because adenosine slows the AV node and exposes residual antergrade accessory pathway conduction? Is it because adenosine facilitates dormant conduction over the accessory pathway? Does adenosine slow the AV node and exposes a bundle branch block? Does adenosine cause accelerated automaticity in the damaged pathway, or is the widening of the QRS complex have nothing to do with the adenosine administration? So we're pacing the atrium at a constant cycle length of 800 milliseconds, and we give adenosine, and this happens. What's going on? Why does that occur? Does adenosine slow the AV node exposing residual accessory pathway? Is adenosine facilitating dormant conduction over the injured accessory pathway? Is adenosine slowing the AV node and exposing a bundle branch block? Does adenosine cause accelerated automaticity in the damaged pathway, or is the widening of the QRS complex have nothing to do with adenosine? All right, here's the tracing. Stop the tape and examine this carefully, if you want. I'm going to pause and then continue. So let's look at the answer. The answer is actually adenosine is making accessory pathway conduction better. So the hyperpolarization effects of adenosine is making it better. Why isn't it just slowing the AV node and exposing the accessory pathway? Well, it's because the stimulus to V interval actually shortens with adenosine. And you can see that the local AV interval, for example, in this CS lead, for example, all of a sudden gets very short. So it's not that you're slowing AV nodal conduction and exposing slow conduction over an accessory pathway. You're actually stimulating conduction over the accessory pathway with adenosine. So if this were slowing of the AV node to expose residual antigrade accessory pathway conduction, the stimulus to QRS interval would prolong or be unchanged. Because the stimulus to QRS interval shortens, the accessory pathway conduction must have improved due to the hyperpolarizing effects of adenosine or dormant conduction. The subsequent slide, which I'll show in a minute, shows disappearance of the delta and prolongation of the stimulus of the QRS interval as adenosine washes out. And as most of you know, you've seen this phenomenon for pulmonary vein exit and entrance, because we commonly use that to test for dormant conduction in or out of pulmonary veins after isolation. And we can also see this dormant conduction enhanced by adenosine after CTI line for atrial flutter. So this is the washout of adenosine. You can see the delta wave gradually disappear. And if we look at a faster sweep speed, you can tell that all of a sudden this close AV interval prolongs. So the accessory pathway conduction actually fails as adenosine washes out. It's not a balance between a node and a damaged accessory pathway. So I thought that was an interesting phenomenon and can be used again to bring out pathway conduction. And after we did further ablation in this patient, we gave adenosine and we just saw nodal block. So that dormant conduction alerted us, especially in an epicardial post-receptal pathway that we ablated by cryoablation, which is not as reliable as RF at getting deep lesions and getting rid of these things definitively. It allowed us to know that the pathway was still there and to keep going. All right, I think I can squeeze one more case in here. Pacing after ablation of a post-receptal accessory pathway shows that the ablation has caused complete AV block. No retrograde accessory pathway conduction is present. There's conduction over a second accessory pathway, there's retrograde AV nodal winky block, or there's intermittent conduction via a damaged accessory pathway. So here are the electrograms. We have the five surface leads, we're pacing the ventricle, we have the right atrium, we have proximal to distal hyst, and we have proximal to distal coronary sinus, and we have right ventricle. All right, so the choices are ablation has caused complete AV block, there's no retrograde accessory pathway conduction, conduction over a second accessory pathway is present, there's retrograde AV nodal winky block, or there's intermittent conduction via a damaged accessory pathway. Very good. Here are the electrograms again. All right, so if you want to look at them more carefully, stop the tape. I'm going to pause for a few seconds. And here's the answer. It shows that there's no retrograde accessory pathway conduction. The ablation has not caused complete AV block, we'll show why in a minute. There's not a second accessory pathway, in fact, there's no retrograde conduction. So we're pacing the ventricle, this is high to low, this is just sinus rhythm. So this is the atrial rate is completely different with no relationship to the ventricular pacing rate, and there's no retrograde conduction. So there's no retrograde accessory pathway conduction at around 600 to 550 millisecond pacing. So that pathway is probably gone. Why is there no antegrade conduction? Well, there's no antegrade conduction, because there's physiologic interference with AV conduction, not necessarily AV block. So this sinus beat doesn't generate a QRS, because the pace beat comes earlier. Same thing here, same thing here. So there's physiologic interference with AV conduction, and we can't tell the difference until we stop pacing. And when we stop pacing, we can see that indeed there is AV conduction, although in this particular case, the AH is pretty long, the AV node is a little slow, but there's AV conduction, there's a narrow QRS, but there's no evidence of residual accessory pathway conduction. So in this patient, the ablation is over, and we can go have lunch. All right, so I think my time is up, and I'm going to stop there. I appreciate your attention. I hope this was fun. I hope it was a teaching thing, and that the explanations were adequate. And I think you can see the slides and go back and look at them at a future date as you go through this, if there is something that is difficult to understand. So thank you so much.
Video Summary
Case 1: The best interpretation of the results is that adenosine is making the conduction through the accessory pathway better. The accessory pathway conduction improves due to the hyperpolarizing effects of adenosine. This suggests that the ablation was not yet successful.<br /><br />Case 2: The tachycardia is most likely caused by non-reentrant junctional tachycardia due to isoproterenol. The administration of isoproterenol facilitates the automaticity of the junctional tissue and triggers the tachycardia.<br /><br />Case 3: The best target for ablation is the site of earliest ventricular activation during tachycardia, which suggests that the tachycardia is arising from that site.<br /><br />Case 4: The QRS complex widens because adenosine causes accelerated automaticity in the damaged pathway. Adenosine can enhance automaticity in damaged or ischemic myocardium, leading to widening of the QRS complex.<br /><br />Case 5: The ablation has caused complete AV block. There is no retrograde accessory pathway conduction seen during pacing, indicating that the ablation was successful in eliminating the accessory pathway.
Keywords
adenosine
conduction
accessory pathway
ablation
tachycardia
isoproterenol
automaticity
junctional tissue
target
QRS complex
AV block
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