Well, it's my pleasure to welcome you to San Diego and Heart Rhythm 2025 for the 46th annual meeting of the Heart Rhythm Society. I'm Dr. Feld. This is Dr. Hazegar on my right. And I'm supposed to tell you all that if you've not already done so, please download this HRS 2025 mobile app from your preferred app store. And this is how you can participate in the live question and answer session. So scan the QR code on the screen to access the session's questions and answers. If you are interested, and when using the mobile app, log in with your HRS credentials. And I'll try to review your questions. We will here on this iPad and get your questions to the speakers. I think the first thing we'll do is have the, can we have the first two case presenters and the first two discussants, if you're available, come on up and join the stage here so we're kind of ready. And we'll do that and then we'll switch to the next two speakers and discussants. So without further ado, let me have Dr. Hazegar introduce the first two speakers, please. So hit my stuff, start, okay? Okay, first case will be presented by Hiroshi Nakagawa from the Cleveland Clinic. What's happened? And the discussion will be Gregory Michaud. I don't know if Greg is there. All right, thank you, Michaud, Greg. I'm Hiroshi Nakagawa, Cleveland Clinic. I'm the first presenter for the unknown SBT tracing. So then, oh, they have to scan the code now? I have the Q&A to the audience. I have two Q&A slides, the very beginning of my talk. Can I go, move forward? Okay. Okay, case one, the 71-year-old woman present the episode of palpitation, occurring every other month, lasting several hours each time. Patient had history of the mesenteric artery thrombosis, lupus anticoagulant, so now she's on the warfarin therapy. Okay, here's the baseline EKG. Easy, right? And then, here's the tachycardia. Look EKG carefully, okay? And then, first question, what is the EKG diagnosis? That's all my slide today, okay? So, AVRT, orthodontic AVRT, VT, AT, junction tachycardia, something else? I don't know. I don't care. Maybe put on the PFA, avoid everything, right? All right, you got an answer? You want to look again at the EKG, right here? All right, let's take a vote. One, two, eight. What? Very fast one? Okay. So, EKG is not completely normal, right? And then, yeah, Michelle's saying normal. I'm not sure it's normal or not, but anyway. It's not normal. Okay, so tachycardia. I don't think we have a system for voting, but. Okay, voting, we can get the result of voting? If not, I move on, okay? Oh, loading. Oh, still, it's slow. When there is a narrow QRS, we have to see where is the P wave, huh? Yeah, but don't give answer. Yeah, yeah, yeah. No, no, I just ask a question. There you go. All right, evidently, and the VT, AT, junction tachy, oh, junction tachy is most popular, same as VT. Oh, because of AV dissociation, you think? Okay, anyway, okay. All right. EKG, baseline, tachycardia. Look at here, as Michelle talking about. It's something there. It looks like a P wave appreciation. So, therefore, you see the P wave between the QRS. Importantly, we say VA dissociation. More important, number will be more than A. Means what? So, at least, this not unlikely atrial tachycardia. Make sense? Okay, any argument? No? Okay, thank you. So, all right, so baseline EKG. So, it's, I need the pointer. How can I do pointer though? Oh, here we go. So, the, I put the, kindly, I put the, all the measurement. AH, HB, QRS duration. So, essentially, normal range, correct? And then, actually, before that, we have the catheter and hyaluronate, and then decapolar hyscathera, and the RBFX, okay? And then, for the baseline, means no isoprotein, you know, the infusion. So, RBFX, the constant pacing of cyclin 600, showing like this. This region, apex, and the higher layer. And then, this is tachycardia. Okay, higher layer, this recording, and RBFX. Easy, right? All right, next question. So, what is the diagonals of this narrow QRS tachycardia? ABNRT, ORT, BT, AT, junction tachycardia, nodal ventricular pathway, or I cannot differentiate between the abnormal reentry and the nodal ventricular pathway. Something else, I don't know. I don't care. All right, let's vote. Come back again to the previous slide. Go back, okay. This one? Yeah. Okay. You see, that's his, multiple of his recordings. All right. Let's take a vote, the interest of the time. Can we? Now, okay. Loading. In this kind of a situation, the best answer is I don't know, actually. Then you're fine, you know. Hiroshi, the multi-electrode his catheter, where is the proximal most electrode? Is it right near the AV junction? The his catheter, or the decapole, this study more likely right boundary region, and approximately, it's still his region, and you have nice atrial potential, his other ventricular potential. All right, the audience saying junction tachycardia. Okay, and the second is another ventricular. Still abnormal entry, and then, oh, number seven, you can differentiate the abnormality and the non-ventricular person, okay? All right, here. Is Greg here? He's not here, okay, all right. And then, again, AHHB QR situation is normal, right? During the sinus season. Here's also the QRS. So, importantly, having the octopolar, decapolar his catheter, that is very important, this kind of the complex SVT, to see whether conducting anti-gradually, rate-gradually, during the sinus, of course, conducting from the proximal his down to here, and here's more already right boundary, because you don't see any atrial potential. It's already ventricular site. Make sense? All right. So, here's the RBApex pacing, okay? And then, even the 600 millisecond, relatively long, the pacing cyclines, you don't see the constant VA conduction. Essentially, actually, primarily dissociate. No VA conduction for the baseline. Again, no isoprotein administration. So, during tachycardia, again, you have more B than A, all right? Same as the EKG. And again, you have nice his here. Why we have the multiple his? Because you see the sequence of the his right boundary activation, actually, anti-grade conduction. This is very important, all right, during tachycardia, even the VA dissociation. And then, look at the HV interval compared to the sinus rhythm. Actually, same as, consistent with anti-grade conduction. If HV is shorter, could be VT or pre-cyclic tachycardia, but this is actually very narrow QRS, however, can be VT coming with relatively narrow QRS, but this already somehow excluding a possibility VT, although could be still junction tachycardia, all right? All right, let's go next. So, this is the, in this case, just given a little bit of iso, one microgram infusion. And then, short burst patient from a higher array at the 360 millisecond, reproduced with initiating tachycardia, all right? Here, then tachycardia here. I just showed you a last stimulus speed to the, with a faster sleep speed, right here. Okay, this is the last patient stimulus. Then, is there some age here? Definitely, we capture the age. If zone-driven tachycardia dissociate, but at the pacing, you can anti-grade age, you observe it, right? It's strange, but it does, actually, usually. And then, look at here, you have the one and the two. B, double B. Is this double ventricular response? I don't have the Greg here, so, any, anybody has a comment, this one? Yeah. Can I turn on mic for him? Please turn on the mic. So SVT with VA block has three diagnoses, junctional tachycardia, notoventricular, or AVNRD. So AVNRD to produce a VA block is very rare. Yeah. My limit of 35 years clinical EP, I haven't seen it. Yeah, right. So it's very rare. So it could be only two, junctional tachycardia with notoventricular. I mean, still, you can say never existed. Some of the report from the- So a double response. There could be a dissociation. OK. So double response tells us that it could be AVNRD with a concealed notoventricular fiber, which is not participating. My question is, is this a double ventricular response or something else? See, there's no A after the first beat. And then the second beat is echo of the first beat. So if there is no A of the first beat, it is probably a double response. Although the barbier, it looks like here's, again, antigravity conduction. Here's the right bundle. Right. But if you look at here, here, maybe simply coming the previous spacing down to the slow pathway, to the AVNRD, and this last one go to here, then this could be it's long, a little longer pose. And then, so therefore, could be this is the initiation of the first tachycardia. Again, the end tachycardia, antigravity hits the right bundle of conduction with the same HV interval. Does it make sense? Any comment, Michel, or Greg? No. No, I think we have to see the beginning of pacing to differentiate which pacing is conducting to the H. Don't we have these two options that you indicate? So I've just, you know. Now, if the QRS is exactly similar to sinus rhythm. Yeah, the sinus rhythm during tachycardia, almost identical. Do you think we need to differentiate hill bundle and right bundle? Yeah, that I'm going to. OK, thank you. Yeah. So now during tachycardia, we perform the higher entrainment. Pacing cyclings, the 350 tachycardia cyclings is short enough for 105 millisecond because we're giving more isoprotein to microgram to maintain the stable sustained tachycardia. So the entraining from higher array, I just put all measurement HH interval. All right? Is there any comment due to this one? Greg was not here, so. This is made for Greg, Michel, but OK. Any comment for this one? OK, so the, look at here. Stimulus to his 380. So actually, this is last captured beat, right? Makes sense. So it's more likely orthodontic capture. During the V8 dissociation, nonocular tachycardia, but you can have entrain from higher array. So this is orthodontic capture, right? If you measure the H interval to 70, so definitely capture through the anti-graded slow AV nodal pathway. Makes sense? OK. And then, how about the entrainment? How about the PPI? But you cannot measure PPI atrium because it dissociated during tachycardia. So the PPI measurement from here to here, it's totally nonsense. But importantly, even though nonocular tachycardia via dissociation, it's able to entrain from a higher array through the slow pathway anti-grade. That's very important. If this is a junction tachycardia, unlikely like this. Junction tachycardia is automatic. So indicating you have the x-type of gap, you can enter, all right? So that's the reentrance circuit. Makes sense? Any comment? Atrial extra stimulus from the high atrium, or even from the CS, could be more useful than entrainment pacing. Because then you are very sure whether you have really pulled in the V or not. So that's actually the, but the, so you think the CS entrainment better than higher array because? Because the slow pathway is located in that area. Oh, no, the more, the posterior inferior equilibrium. Yes, right. But at least it was constantly entering the slow pathway because constant H interval 270, which is OK, right? Any comment, Michelle, Greg? No, I think I agree. All right. And then? So able to enter from higher array via the slow avenoidal pathway. I agree. Indicating the relatively large reentrance circuit with some x-type of gap. Unlikely for the automatic junction tachycardia period. OK. This is very important. So how about the RB apex entrainment? I know the 95% people like RB apex entrainment. As soon as you see narrow case tachycardia entrainment. When I was at the University of Oklahoma, actually, we never do that. And then I joined the Cleveland Clinic. Cleveland Clinic, they love the RB apex entrainment. And every Tuesday morning, we have EGM conference. I had to fight with the young faculty, the fellows. But anyway, so this case is the RB apex entrainment. 380 millisecond pacing cycle lengths. Tachycardia cycle length is 295. It's shorter because now the isoprotein is 2 microgram. All right? So make sure that you capture constantly. And here's the PPI. 515 compared to the tachycardia cycle lengths plus 120. How do you judge based on this PPI plus 120? Any comment? I think it's, I don't know how much pacing you did before the tachycardia. But. It's constant capture there. But I'm not sure that if. I think if you're not to your constant pathway, continual ventricular pathway, cannot be differentiated only by that. Because it depends. If you have a tachycardia, you are pacing 10 or 20 times. We don't know exactly how is the relationship between the last pacing and the first QLS post-pacing. And I have another question. I'm struck here by the activation in the actual activation in HB. He's been done 9, 10. Okay, yeah, Michelle there. Okay. During entrainment and the VA dissociation. Yeah. And the PPI plus 120. And the people want to look at the VHV response. But this is totally, you know, associated. Look, now it's not sinus rhythm. It was A. Oh, no, no, this is during the tachycardia. But the A, actually, now his A is earlier than the higher A. There is a capture from intermittent capture. Yeah, exactly. So now sometimes you see not always the shown VA dissociation. Sometimes you see some conduction. However, not impacted the tachycardia. That's also important. Yeah. So 120 means what? ABRT or ORT. It's kind of borderline, right? Yeah, exactly. That's a problem for the RBA-APICS entrainment. Even we just do the only 15 millisecond shorter than tachycardic cyclings, try to reduce the producer conduction there within the circuit. But even so, 120, it's kind of inconclusive. All right? I know some publication up to 125 OK, but it depends on RBA-APICS where pacing. That's also a problem, though. But anyway, finally, my discussant, the professor that we chose, shows up. OK. I was afraid of you. OK. He doesn't like me, so anyway. OK. He's actually a guy who invented the RBA-APICS entrainment to differentiate the mechanism. So Greg, you have to answer this one. Let me explain. Narrow-case tachycardia, VA dissociation. So during the tachycardia, following your idea, so RBA-APICS pacing, like 15 millisecond shorter than tachycardic cyclings. This is the return beat. PPR is 515. That is actually 120 millisecond longer than tachycardic cyclings. What is your diagnosis based on the technique that you proposed like 20 years ago? This is ORT or abnormal entry, or you cannot tell? Well, you're dealing, so you're doing V, so in other words, you don't have one-to-one conduction retrograde, no? For the atrium, yeah, usually dissociate sometime in the weak conduction. Forget about A right now. Yeah. So, I mean, I think when, then you're wondering is there a notophysicular fiber, something that doesn't require the atrium? It's ORT's out the window because it requires the atrium. And then you could have AVNRT. For notophysicular, you should be able to drive the hiss orthodromically. So your entrainment should require that the next hiss comes at the pacing cycle. Or that would be, that would be what I would be looking at. So if your post-pacing interval is long, it's probably more consistent with AVNRT still, even though you're not looking at what's happening in the atrium anymore. So there's no VAV to look at, there's no any of that. But the post-pacing interval can still be useful because you're looking to see whether the circuit might still be below the node and involve the ventricle or the fascicles in some way, so. So the best publication, the like a plus 150 or 110 is like a cut-off line. I don't remember the exact number. One, one, five. One, one, five. So this is more consistent with the AVNRT, based on this one. So make sure that you're not pacing too fast. Only 15 minutes can show that type of cycle length. For me, it's inconclusive. Could be either way. So then, here's the another one. So during a tachycardia, we got a spontaneous PBC or just maybe cast the banking from the apex. All right, then. Actually, the, I was just measuring HH interval. After the PBC, HH interval prolonged 20 millisecond. Okay, interesting time. I might go right here. So this could be his refractive PBC because you can tell the, his right bundle is still under conduction committed. It's no way to go up to the AV node, correct? Also, you don't see much of the VA conduction. But the, his rectal PBC delayed next his bundle, 20 millisecond. And if you look at the RR interval, double, 760, 78. So his rectal PBC advanced next, actually not advanced, delayed the next V. His actually, his and V. So is there any comment for this one? Yeah, can I make a comment on this? Yeah, go ahead, please. If you delay by his refractory PBC, prove two things. First, it's a pathway. And second, the pathway is participating in the tachycardia. And with this evidence that you have of the next his, it tells you that it's more like a notofascicular. So again, the his rectal PBC affected the next his. Either way, advanced or delayed, it doesn't matter, affected. And also at the same time, the receding tachycardia. So therefore, his refractory PBC delayed next, in his 20 millisecond, receding tachycardia, already confirming a lot of stuff. Yes, presents the reticulated accessory pathway connecting AV node. And this accessory pathway participating tachycardia, period. So we don't need RVX entrainment. We're just PBC. We're just energy-saving. We don't need much electricity, okay? Just one PBC, or just a spontaneous PBC. So summary, narrow-cure tachycardia with a BA dissociation, identical aqueous morphology to the cures during the sinus region. Variable cycle length is sensitive to isopretinol. During tachycardia, importantly, antiviral conduction hits right bundle with the same HV interval during the sinus region. Atrial pacing entrained tachycardia via the slow pathway. RVX entrainment of tachycardia, yes, but the PPI plus 120, is kind of the borderline inconclusive. But most importantly, his refractory PBC delayed next hits and receding tachycardia. So therefore, this narrow-cure tachycardia, antiviral limb, slow AV nodal pathway, retrograde limb via the conceded non-ventricular pathway. So since AV nodal pathway, slow AV nodal pathway involved within the entrance circuit, based on the atrial entrainment, so RF aberration, not PFA, okay, was performed, targeting the slow AV nodal pathway, i.e. the right water inferior extension, i.e. usual area between the CSOs to the tricuspid anus. Also, we're extending toward the more ventricular side, try to attempt to ablate ventricular insertion site of the nodal ventricular pathway. During RF aberration, we see a lot of junction reason, however, no VA conduction, VA block. It seems scary, however, baseline no VA conduction, no way to see the VA conduction. So as long as aberration site very inferior, you should be fine. Okay, and the post-aberration, tachycardia was no longer induced, despite the isoprotenol. Still, antiviral pathway conduction, but no ECOBEAT, and antiviral ERP is 320, one-to-one conduction up to 540. And finally, surprisingly, end of procedure after aberration, we recognize weak retrograde conduction with isoprotenol, one-to-one VA conduction with the patient's cycle length 510. So like this, schematically showing, this is Anton Baker's schematic showing the AV node, rightward inferior extension, his bundle coming here, and also important, you see transition cell distribution. Proportionally, the entrance act like this, goes through the antiviral pathways through the right inferior expansion and the history bundle coming back here. Here is a famous nodal ventricular, conceded nodal ventricular connection. So this is Dr. Enford's slide, kindly she gave me. So here's again, schematically showing the slow pathway here, fast pathways, nodal ventricular connection. She also showed AV node, very posterior inferior, you see the nodal ventricular connection. By the way, this patient no history of palpitation, but this is based on the histology. Thank you. Thank you. Thank you, great case. Yeah, I'm sorry that we're gonna have to move on because we're already at five minutes over to deal with all those questions, but we'll try to move along, have a few at the end. So we'll do the second case now. Now, the second speaker will be Ricardo Capato. And the discussion will be Balbir Makar. Thank you. So, good morning ladies and gentlemen, Mr. Chairman, it's a great honor to be here in front of such a large audience. I would be very happy, I will only show you a few slides, but I would be very happy if I was able at the end of the presentation to fix in your mind the peculiarities of these EKGs. They are not common to be found, but if you fix them in your mind today, next time you are going to find them, you will recognize. So I have only four tracings, please get very focused on what you are going to see. The first slide is split into two parts, on the left side there is a narrow QRS tachycardia with a wide QRS in V1, possibly mimicking a pre-excited beat, which is not replicated in other leads. The heart rate is 165 beats per minute, there is no clearly visible P wave, and there is a bifascicular block configuration, compatible with right bundle branch and left posterior fascicle block. On the right side, the same young patient, I'm not going to give you clinical data about the patient because they are relevant for us to possibly introduce the type of arrhythmia we are talking about. We will do it at the end of the presentation, and that is also a kind of information that can be associated with the very specificity of this arrhythmia. During sinus arrhythmia in this young person, you may recognize that there is some alteration in the repolarization, indicative of a non-entirely normal condition, with a T wave which is negative in 2, 3, and AVF, and tends to be negative in V4 to V6. Now you may certainly appreciate the very different axis that the QRS is presenting during sinus arrhythmia and during tachycardia. I think our first question is, based on the QRS configuration during tachycardia, is it going to be a supraventricular tachycardia, a narrow ventricular tachycardia, or some form of unusually pre-excited tachycardia? So next, can we go back to the slide? Absolutely. So if we look at the sinus arrhythmia ECG, we see the axis is normal, and then you have a shift of axis. And if you look at V1, it's not an RBB pattern, there is a slight delta which is seen. The QRS is narrow. The QRS is definitely narrow. The P wave relationship is not seen. The axis has changed significantly. So SVT with aberration does not look like, because there is no initial R and the R vector in V1 is all positive, with a mild delta which is seen. And with such a shift in the axis, it favors a ventricular tachycardia more than SVT. But SVT can be there if we believe that it could be arising near the junction and producing this kind of, on the left side. But it's more like a VT to me than an SVT, even though the session is SVT, so, but I'll take that. So I'd like to come back to something like 40 years ago and ignore if we have technology here and use an old-fashioned way. How many of you do believe this is a ventricular tachycardia based on what we have seen on the EKG and the wise comment of our chair? Please raise your hand those who believe this is V ventricular tachycardia. Those who believe this may be supraventricular tachycardia. So I would say 80% are not raising their hands. You're shy, aren't you? Or you don't know anything about electrophysiology. Of those 20% who've raised their hands, the majority were in favor of ventricular tachycardia. So our chairman is a good politician. I think he should start considering this career. Now this is what happens during atrial stimulation, programmed electrical stimulation. So clearly the patient came to the EPI lab, underwent programmed electrical stimulation, and during pacing from the high right atrium with an S1, S2 preceding atrial beat, this is what happens. And I highlighted for you the QRS configuration that could be visible at the time when the arrhythmia was induced. I think the chairman and the audience would all agree that the first premature atrial extra beat is responsible for the activation of the QRS morphology highlighted within the blue picture. But what happens for the second, which is highlighted in red, is relevant for two reasons. For one, it shows an immediate change of the QRS configuration from sinus to tachycardia. Exactly of the same type as we saw during natural conditions of sinus rhythm and clinical tachycardia. Please appreciate, although we only have six EKG leads in this picture, that the QRS configuration highlighted in blue is compatible with the configuration observed in sinus rhythm, and the one highlighted in red is compatible with the configuration observed during tachycardia, spontaneous tachycardia, in this subject. You may also be close enough to the screen to appreciate that while there are few doubts, the first QRS highlighted in blue here is activated by the S, is likely activated by the anticipated stimulus. The second one is of questionable origin. And I would like to give you an answer to the pending question, except raising the doubt that an atrial re-entrant beat being originated and more visible at the level of A1, A2 in our atrial mapping catheter, may be responsible for the second beat. But if the second beat is originating by an atrial second extra beats, and it's wide QRS morphology in V1, and the many considerations made by our chairman makes us, at least the majority of us, believe that this is a ventricular arrhythmia, is that sequence that we are observing in this slide compatible with an immediate shift from an atrial extra beat to the first beat of a ventricular tachycardia? Now I want to go to this. So I leave the question open at this point in time, and I go to the third slide. The third slide is taken during ongoing arrhythmia and is relevant for two reasons. Reason number one is, during proceeding from the atrium, you have an anticipation of the next QRS complex. And most important, and apparently unexpected, is that his bundle deflection recorded at his location is within the QRS complex. So we go back. Remember this is a morphology of the QRS during tachycardia, supraventricular, ventricular. This is a morphology of the induced tachycardia after atrial extra beats. This is the consequence that atrial proceeding produces during ongoing tachycardia. Please. Again, you have a nice history recording, so therefore this is wide QRS tachycardia. First I look at the adrenal sinus rhythm, HIV interval, compared during the wide QRS tachycardia. If the HIV is shorter than sinus rhythm, that's actually BT or pre-excited tachycardia. So that's actually having a nice history recording like you have, that's answering a lot of stuff. To be honest, I'm not good to differentiate based on the QRS morphology. For me, way complicated. But just measuring HIV interval during sinus rhythm and during wide QRS tachycardia is quite useful. Do you have any comments? It's negative, right? So what is your conclusion based on that? So if there is a negative HV interval and the H lies within the first 30 milliseconds of the QRS, it generally involves a fascicular system, generally involves a fascicular system. So to me, it is not an antidromic tachycardia. We don't see a pre-excited ECG, so it has to be a VT, which involves a fascicular system. Hiroshi? Yeah, that's more likely, but even Bear Hudson, there to be his recording, but usually after the QRS. Within the first 30 minutes. Yeah, usually 30, 40 milliseconds. It's related to some pre-kinged system, automatic or re-entry, it doesn't matter. I didn't understand. SVT or VT? So not SVT. Based on this one, not SVT. So if this is SVT, I need this slide for my collection. I, you know, remember when I started, I told, I want you to keep very, very concentrated on these slides because there are unusual, but once you have fixed them in your memory, if you find them again, you will not forget them. Here is the last slide, last tracing. Now what happens here is something very surprising, and by the way, I would say diagnostic. So take 10 seconds of silence to look at it. Now what you appreciate on the left of this slide is activation sequence and the QRS morphology that we were used to say in sinus rhythm in this patient. That what we do here, we paste from the right posteroseptal region of the atrium. I'm sure that everybody is appreciating that there is an artifact followed by a P wave, not by a QRS complex, and that the P wave shows a negative morphology in 2, 3, and AVF. And what happens then in response to pacing from the right posteroseptal region is an abrupt change in the QRS morphology as compared to the spontaneous QRS morphology, which is indicative of a change of penetration into the ventricle. How can we, and by the way, the QRS morphology that we observe in response to pacing from the right posteroseptal region is of the same type in 12 lead perspective of the type that we are experiencing during tachycardia. Isn't that? And that is very confusing, isn't that? So if there are no other comments from the chair table, I would come to the conclusion, provide you with the two imaging slides that I have available. This is first. I have a question. Did you map the earliest ventricle activation here? What is the insertion of the ventricle when it's a white QRS? Yes, we did. And to frankly expand my answer to your question is, I was asked by the organizers to only limit the number of slides. So they were available. And to expand on the implicit question that you are making, there were no changes in terms of how the ventricle, the H to V ventricle was calculated during sinus rhythm, and there were major changes when we were pacing from the posteroseptal region. So assuming that there was a different level of activation. Please. Was there any change in the degree of pre-excitation when you paced the faster cycle lengths? It looks like the pre-excitation, the degree of pre-excitation is fixed. No differences. When you pulled in that one beat with atrial pacing, it didn't change the degree of pre-excitation. It didn't? It pulled in the hiss as well. So this is a funny connection. This isn't like a normal AV type of connection, just because the pre-excitation doesn't change. It's more like the type of fiber where you see a fasciculoventricular. This isn't where you usually see them. Can I respectfully ask you, why are you using the term pre-excitation here? Do we have any conclusive evidence? What we have is, and I would agree, that I showed you an EKG in which the AV node comes after the QAS during tachycardia. But I think we have not conclusively proven that this is a pre-excited tachycardia. We have said that the QRS is wide in V1, mimicking the pre-excited, but we have also identified a left posterior fascicle block in 2, 3, and AVF. So let me, is there anybody here that has in mind what could be the final diagnosis for this patient? You know, remember, this slide to me is conclusive and is diagnostic because it is through a normal AV interval after pacing from the right posterior septum that we obtain the QRS morphology as during tachycardia. So this is not a pre-excited tachycardia. And the QRS that we see in V1, please take a look here, is mimicking a wide QRS complex, such as a pre-excited complex, but is following a totally normal stimulus to R interval. And therefore, I would conclude that this is a bifascicular block-type configuration. I would agree with our chairman when he said this is not a typical right bundle branch block morphology. And this is another key message for you to take home, how peculiar this EKG is. So this is the X-ray view from left anterior oblique perspective. The normal AV nodal position is obtained from the aorta. The right posterior septal and the low right atrium positions are obtained through a fenestrated hole of a fontane in a young lady with two AV nodes. So what happened? You didn't tell us. You have to tell me. You have to tell me in advance this condition. It's not fair, though. Is it not fair because you were not able to answer, or what? So this is a macro-reentrant tachycardia. We have a twin node situation. We have, I would say, a congenital disease preventing the posterior AV node to migrate during the embryonic phase to the anterior region and set into the final position. And we have an anterior node which is going to mature and evolve at a separate anatomical level. So this is the anterior node, and this is the posterior node. What happens during normal sinus rhythm is activation of the anterior node and penetration of the anterior and posterior bundle of the left fascicles simultaneously. What happens in response to the HLX beads, and I would say, by the way, in response to the second spontaneous atrium, which is observed after stimulus anticipation, is penetration through its block of the anterior node and activation of the posterior node such that integrate penetration through the posterior fascicle and to the right bundle is made available and re-entry occurs. The antegrade limb being represented by the posterior node and the retrograde limb being represented by the anterior node. Please note that penetration of the electrical impulse into the ventricles retrogradly enters the anterior fascicle, making, therefore, possible penetration during re-entry of the antegrade penetration during re-entry of the anterior fascicle unable to compete with the posterior fascicle, and therefore, justifying the left bundle, the posterior fascicle block position. So the recovery, so this is essentially the antidromic, the tachycardia. So therefore, short HB, negative HB still works fine, although you don't have the excitation because second AV node, but that's accessory AV node, accessory pathway. So still short HB is, you know, differentiating the SVT anterior conduction. So it's still okay, though, HB criteria. The HB criteria are consistent and compatible, but what we didn't have available because of the restrictions of the anatomy in these patients was the simultaneous recording of the HB interval from the anterior and the posterior node. Should this be available, we would have been in the perfect position to provide you with all the elements, not to be disoriented at the time when we were showing the tracing. So I want to thank you very much for your attention. Great case. Thank you. So what we're going to do is have the current speakers and discussions go ahead and sit down, and then the next set of speakers and discussions come on up to the podium, please. Thank you. And I'll present the next two speakers. So the first case will be presented by Dr. Waleed Saliba from Cleveland Clinic, and the discussion will be Isabel Nault. That was intense, so I thought the session was for challenging cases, not impossible cases. Okay, so full disclosure, all the presenters were not supposed to talk to each other and we did not know who is presenting what and what kind of cases are being presented. So that is your hint for today. So this is a 45-year-old man with recurrent narrow QRS tachycardia. By the way, my slides are very simple. It's none of this esoteric things. So that patient had three EP studies and in the reports they said that they induced AVNRT with one-to-one VA conduction and tried to ablate the slow pathway several times but were unsuccessful to actually abolish the tachycardia. The third attempt, last time, he resulted in VA dissociation during tachycardia, again hint for the first case, and PR prolongation and sinus rhythm. And this is the baseline EKG that we have. So the baseline EKG shows, as you can see here, everything is normal except for the PR, which is 260 milliseconds after the third ablation. Went for the EP study and these are the baseline intervals. That is not a trick question. Baseline intervals are normal except for first-degree AV block. We just put a quad in the HISS, no decoupler, on the assumption that we're going to have AVNRT and we're going to be successful in ablating it. And because also Hiroshi moved from Oklahoma to Cleveland Clinic, now we're starting to put high-right catheters and we are not pacing the RV apex as much anymore. Well, we'll try to. Anyway, so AH182, HV44, no problems. Ventricular stimulation induced tachycardia. Look at it for a little bit. OK. So what is the first thing that strikes you? Yes, exactly. John got it right. VA dissociation. So there's VA dissociation. So we're back to this differential diagnosis of narrow complex tachycardia with VA dissociation. And what is the differential diagnosis? VT would seem unlikely. Okay, so as we said there's AV dissociation and therefore I think the differential diagnosis is either Junctional tachycardia. By the way, I don't believe in junctional tachycardia in adults. It's in the pediatric patient population AV node with upper common pathway block Anatomically for me, it doesn't make sense ORT with ventricular nodal ventricular hyssian accessory pathway or Or Some minor variation may be in the QRS complex would get you into an upper septal fascicular VT But this session is about SVT and the S is not for sustained VT is for supraventricular tachycardia So Contrary to what dr. Nakagawa wants we did VOD from the RV apex Assuming that this is the differential diagnosis and I'm going to try to I'm gonna try to show a couple of things to at least guide you as to how ablation for these kinds of Tachycardias how we approach these in at least in the EP lab, so this is VOD from the RV apex and I put some numbers here So you have the I can put let me see the numbers, okay, here you go, I put some numbers here So you can see here that we're pacing from the ventricle And These numbers here are the HH intervals and Down here is obviously the RV pacing from the apex and the return post pacing intervals Do you Notice something or do you see something you can have good his electrograms so you can measure the HH So what you can see here is that while pacing from the apex? I mean, this is an H but the last entrained or the last H that is pulled to the pacing cycle is Actually this one over here So you have This is going here. This is going here and this is going here and your point post pacing interval is 330 millisecond and if you go through the usual Calculations post pacing interval minus the tachycardia cycle length is 40 millisecond not 110 or 105 40 millisecond. What does this tell you? This is the apex? I Mean Does this Tell us whether this is the possibilities that we're having can this be a node of ventricular or Or his ventricular fibers Well, the apex is Almost part of the circuit. It's very close to the circuit and while we pacing from the Apex we are bringing in the next hiss at 270 millisecond so it'd be more likely towards a Non nodal maybe towards a pathway So that is that is one of the possibilities and then Hiroshi showed us a slide whereby a fortuitous PVC actually delayed his activation This is the other way around a fortuitous PVC in this situation Brought in the next hiss Which implies that there is some kind of accessory pathway present because The PVC from the apex at the time where the hiss PVC at the apex at the time where the hiss is refractory is Affecting the next hiss so it has to be going up via a certain pathway That we commonly call accessory Well in the previous slide was the HV interval varying was much shorter So the HV interval actually in this location where the catheter is is not is not shorter Necessarily, but I will come to that because that is interesting So Where there is evidence of an accessory pathway and that brings up actually most Commonly the possibility of this is a ventricular nodal or a ventricular hissing pathway now what since we've heard about all these possibilities and how you differentiate between The differential diagnosis that we have maybe I'm gonna twist the my presentation to talk to you about you know How do you map these and how do you ablate those accessory pathways if you found that? okay, there is an excess there is an accessory connection and it is possibly inserting in the AV node or distal hiss and what what gave it away is essentially if you look at the hiss activation actually here You can see that the hiss activation might not be as is that in this slide or in this slide Might not be this one. So even though the HV interval is normal or maybe slightly Shorter but the The Propagation of the hiss is can be or It's possible for it to be distal to proximal rather than proximal to distal but we don't have all the hisses here that for to judge that and I wish that we had like what dr. Nakagawa presented a ten-pole hiss in this location so that you can see very importantly if the hiss is anti greatly retrogradely or actually Chevron kind of Activation because this is how you know where the insertion site of those pathways are but having said that What we do is sorry, what we do is we Try to entrain from different sites Because there is no way for you to know where this accessory pathway is inserting But there are common sites where those pathways can be It's either under the hiss Or above the hiss or on the left side on the LV septum So your best bet is that you need to Entrain in those areas and see which one gives you the best entrainment So this is entrainment from the base of the septum again The tachycardia is cycle length is different because of isoprol effect and what have you But what you can see here is you can probably appreciate that the tachycardia cycling is 340 pacing cycle length is 310 and Your PPI minus tachycardia cycle length in this location is 25 millisecond better than the apex Which is not surprising To the point that actually now at the Cleveland Clinic whenever we have a tracing that is suggestive of AVNRT We do not assume it's AVNRT just because of the intervals We pace we overdrive pace from the apex and we overdrive pace from the base Just to make sure that your PPI minus tachycardia cycle length at the base is longer in cases of AVNRT and shorter in ventricular nodal fibers so in this situation, this is shorter and you go to the left side and you try to pace from right under the coronary cusp right coronary cusp and You see here that tachycardia is at 290 millisecond Pacing cycle length is 250 millisecond and your PPI minus tachycardia cycle length is even shorter 10 millisecond because you cannot afford to ablate in all those areas. You want to choose the best area to try to get to these pathways and This is essentially where we ablated. These are the hiss so away from the hiss Right under the right coronary cusp you deliver ablations and you try to induce and that goes away. So I Know that we did not I wanted to go through the discussion, but Hiroshi actually discussed all these Possibilities at the beginning, but what I wanted to show you is essentially Good old electrophysiology ladder diagram These are the ventricular nodal fibers or ventricular hyssian fibers in the situation where you can have retrograde up the accessory pathway to the AV node and you can have Actually VA conduction and that can mimic very much AV and RT because the V and DA are very close to each other so AV and RT actually can be what you think is AV and RT can be ventricular nodal fibers and I can tell you that Maybe some of what we call upper common pathway block because of VA dissociation is actually AV and RT is actually ventricular nodal fibers and It so happened that for example this situation you can have VA dissociation, but it's so happened if you see where do we ablate those? This is for example Accessory pathway inserting into the AV node right under the bundle of hiss. Well, this is where we ablate usually the slow pathway so Sometimes you might be ablating ventricular nodal fibers if you start right at the annulus without essentially knowing that we are ablating ventricular nodal fibers and sometimes of some of those very odd or Difficult AV and RT is that we see Essentially our ventricular nodal and then we need to go slightly distal But in this situation as I said, it can be under the hiss but also on the other side it can be Above the hiss kind of an interoceptive region and on the left side. It can be right under the right coronary cusp Away from the hiss like more posterior than the hiss and You have to entrain from this location to see which one gives you the best entrainment so that you can ablate in in those location Which is the concept of intra atrial re-entry. I have one last slide that I want to show you and Well, actually not Two more slides so when you suspect ventricular nodal ventricular hiss in re-entry when the 12-lead EKG shows VA block VA dissociation during tachycardia and As dr. Feld said when the HV during tachycardia is shorter than during sinus This means that the insertion is actually probably at the hiss region With RV apical pacing as I said the PPI minus tachycardia cycle length is less than 120 milliseconds Which tells you that that part is within the circuit probably? RV or LV basal pacing sites near the his bundle shows progressive fusion with a PPI minus tachycardia cycle length is near zero and PVC during his refractoriness disturbs the hiss as dr. Nakagawa show you it extends it or it pulls it in So one more I have one more slides ablation pearls for the true of These path where ablation of these pathway there is no activation mapping possible you've as I said you find the sites that has the best entrainment and post-patient interval, and ablate in that location. And you target these sites for ablation to try to interrupt the conduction of this pathway. Now, you have to watch for your ablate on the right side for new right bundle branch block. So as you ablate, make sure that you don't have an R prime that is growing in V1. And you watch when you ablate on the left side that you're not getting widening of the QRS, which is developing of left bundle branch block. Thank you. By the way, this is in memory of Dr. Pat Chu, who is the great master. And we actually compiled a lot of cases of ventriculonodal. These are some of the manifestation of ventriculonodal fibers. He's the one who actually ablated AV block, the patient who came in with the AV block, secondary to a ventriculonodal pathway. He ablated the pathway and relieved the AV block. So these are the different manifestations that you can see with ventriculonodal pathway. And just for your information, thank you very much. Thank you. Thank you. I want to keep us on time, but I think we might have time for one question. Thank you. So that was a great presentation. You mentioned that his activation. In your first slide, you have his prox, distal, and mid. And distal is earlier than prox and mid. This is why I said I didn't want to give it away. I passed through that slide very quickly, but you are right. There is retrograde activation of the his. This is why this case is not really a ventriculonodal, but mostly a ventriculohysian pathway. The insertion is into the his or even a distal. So the whole concept of infraatrial tachycardia is you have AVNRT, you go down, you have ventriculonodal fibers. If the circuit is slowly further down, it's ventriculohysian. If it's even further down, it's upper septal fascicular VT. Hence the reason that Hiroshi puts the multipolar his. We do, too. It's very helpful. Every time we have this, Hiroshi comes and ponders us that we need to put a decoupler at the his. So what a very nice case. I want to argue, again, like every Tuesday, my EGM conference in Cleveland Clinic. So then, talking of dendritic tachycardia, still VH long compared to HV, right? Looks like it's still using the anti-grade slow pathway conduction. As you know, the recent Japanese group proposed that slow pathway can be connected superior and above the his. So that could be still using anti-grade slow AVNRT conduction for your case, I believe. And then, in order to differentiate, if within the end circuit, you have the AVNRT even just shorter than tachycardia, you produce the tremendous conduction delay sometimes. No prediction, OK? So therefore, they're delivering the late PVC, of course, after the his activation. So later PVC advance or delay next his compared to the post receptor basal or antireceptor basal. And in this case, should have the differentiation. So again, in treatment, if the end circuit involving AVNRT, tremendous conduction delay, PPR is sometimes tricky. It's based on the case. Do you have any comment? Yes. So I think in this situation, the slow pathway is not necessarily part or participating in the tachycardia and proving. He had three ablations for slow pathway. No, no. But a slow pathway, you have not only right inferior extension, left inferior extension, left inferior extension, also superior anterior. So that's a network distribution, the transition cell. So the slow pathway is not always the right post receptor. I think the decrement in this circuit here is the accessory pathway connecting to the his region. This is where most of the decrement is happening. And this is why when you want to pace not too fast, not much faster than the tachycardia cycle length, because that can disturb. And then you might have a false PPI minus tachycardia cycle length. But there's no way for you to map this, except by doing PPI minus tachycardia. Like we do the Lulang-Abeno re-entry, you can do the rate PAC for the undergrad being right inferior extension or left inferior extension. We can differentiate. We can do the same stuff. Yes. Single PACs, yes. OK, so we have one more comment from Dr. Hasegawa here. Go to the next speaker. We had an interesting story. We had a case like that in the past. And the patient, when we did mapping, and we found this nodal ventricular pathway involved in the tachycardia, we said, OK, we can ablate that. But the patient said, I want zero risk of heavy block. I said, OK, this is a bit difficult, given the proximity to the heavy node. And during tachycardia, we inject some flaconide. And the flaconide block exactly on the pathway. And we, OK, don't we give the patient flaconide. And for a long time, we had no more tachycardia. So again, a 1C agent to block the pathway, but not slow the heavy node with a nodal blocker. All right, let's go to the last speaker. Then Director Reginald-Hull is going to give us a talk on his, I guess, an SVT case, hopefully. And Dr. Stevenson will be the discussant. Thank you. Good morning, ladies and gentlemen, it is a pleasure to be here to present the case of a 75-year-old woman with recurrent symptomatic supraventricular tachycardia who underwent diagnostic EP study. At baseline, she had retrograde VA conduction that was earliest at the anteroseptum and decremental. Programmed atrial exostimulation induced the following SVT, which had earliest atrial activation along the anteroseptum that was simultaneous with the ventricle, excluding orthodromic reciprocating tachycardia using an anteroseptal accessory pathway. A his refractory VPD terminated tachycardia. But it terminated tachycardia in an unusual fashion in that it did not affect the immediate atrium, nor the subsequent his bundle, but atrial activation one cycle later. We thought that this simply might be a coincidence. So we reinduced tachycardia, delivered another his refractory VPD, but got the same finding, indicating the presence of a bypass track, and effectively excluding an atrial tachycardia, junctional ectopic tachycardia, and pure typical AV nodal reentrant tachycardia. We felt that the most likely diagnosis was typical AV nodal reentrant tachycardia with a concealed bystander nodal pathway, a nodal fascicular or nodal ventricular accessory pathway inserting into the FAST pathway. In this scenario, a his refractory VPD that is delivered nearly simultaneously with retrograde FAST pathway conduction during ongoing tachycardia would not preempt the immediate atrium, but could conduct slowly over the nodal bypass track into the FAST pathway, rendering it refractory downstream and terminating tachycardia one cycle later. We reinduced tachycardia, gave another his refractory VPD, but instead of terminating tachycardia, it transformed it to a different longer RP SVT, which now had earliest atrial activation along the posterior septum, positive P waves in lead V1, and negative P waves in lead I, indicating atrial origin from a left-sided posterior septal structure. And this was a reproducible finding. So in order to determine the mechanism of the second SVT, we also delivered his refractory VPDs, which terminated tachycardia one cycle later, just like it did during typical AVNRT. And this was also a reproducible finding. So we hypothesize that in a patient with typical AV nodal reentrant tachycardia, with a concealed bystander nodal pathway inserting into the FAST pathway, a his refractory VPD blocks retrograde conduction over the FAST pathway, switching retrograde conduction to a left-sided slow pathway, and converting typical slow FAST AVNRT to an atypical slow slow AVNRT with left-sided inputs to the AV node. These left-sided extensions to the AV node were also associated with a second concealed nodal bypass track that allowed his refractory VPDs to terminate tachycardia one cycle later. Common to both tachycardias is the antigrade slow pathway, presumably the right inferior extension of the AV node, which we therefore targeted for ablation, got slow junctional rhythm with 121J conduction, and which rendered her tachycardias non-inducible. And she has been symptom-free for over three years. Thank you for your attention. Thank you. Thank you. So it's interesting that one, so one ablation site abolished both tachycardias, and since there are two pathways for slow conduction, you could have gotten unlucky and had a second inducible AVNRT, but she clearly didn't have that. That's an amazing case. Thank you, thank you. You didn't show us any ventricular entrainment. Did you try that? Yeah, so we did entrainment, got long post-pacing intervals, and the same, I guess, findings that you would have typical AVNRT with an AV response and long PPI. So they weren't too helpful, and that's why I didn't show it, and probably Dr. Nagagawa would probably be upset for showing entrainment also, so. Did you do any atrial entrainment? So we gave, actually, she had spontaneous APDs from the high-rate atrium just during tachycardia that terminated the first SVT with AV block that was his refractory, so we had a kind of good understanding that this was typical AVNRT and not junctional ectopic tachycardia, but we didn't do entrainment from the atrium. Yeah, wonderful case. So there were a couple questions in the audience. Maybe I can ask those. First one says, well, did you ablate during sinus rhythm or tachycardia? Ablated during sinus rhythm, generally for slow pathway ablation, I like to ablate during sinus rhythm and assume that she would have a good VA conduction, so we ablated during sinus rhythm and got retrograde JA conduction. I'm gonna follow that on with a question. Did you ablate approximately in the usual slow pathway position or also further down the angle? Oh, yeah, the same proximal, got a small fraction at A, large ventriculotogram, and fortunately, that was the successful site for both tachycardias. So in fact, that took out the slow pathway contributions to both tachycardias. Correct, correct. Here's a second question. Can you open window map this? Did you map the insertions during? Good question. I don't know if we, obviously, do a lot of open window mapping for accessory pathways, but for AVNRT, I'm not as aware. Certainly, there's the late activation wavefront collision that we started to do, and then the low-voltage bridges, which we didn't do in this case. We just mapped the classic electrophysiology, but those are other mechanisms to map the slow pathway. Yeah, well, when you have an atypical form of AVNRT with a long VA interval, if you can get that to conduct well, then you can map that during ventricular pacing and find the location of the atrial insertion of the slow pathway. Maybe that's what they were thinking of. I guess in that situation, then we'd be ablating on the left side, and we would get rid of the atypical slow AVNRT, but we still have the typical slow-fast AVNRT that uses the right inferior extension of the AV node. Fortunately, the right inferior extension was involved in both mechanisms, so that eliminated both tachycardias. All right, great, wonderful. Well, if there's no further questions, I guess we'll end this session on time. After all, thank you very much. Thank you.

supraventricular tachycardia

Heart Rhythm 2025

EKG analysis

arrhythmia

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warfarin therapy

electrophysiology

entrainment pacing

dual AV nodes

fascicular pathways

ablation strategies