Good afternoon, everybody, or late morning. This is great. I'm looking forward to this session a lot. My name is Zach Goldberger from the University of Wisconsin-Madison. I'm joined by my co-chair, Dr. Vasilios Vasilikos from Master and Aristotle Hospital in Thessaloniki, Greece. Panelists include Dr. John Fisher from Montefiore, Einstein Medical Center, and Dr. Neeraj Varma from the Cleveland Clinic, Dr. Mel Scheinman from UCSF, Dr. Sergio Pinsky from Medical University of South Carolina, and Dr. Hari Tandri from Vanderbilt University. So this is going to be sort of an ECG review. There will be no EGMs shown in this session. Dr. Robinson will be doing an EGM review next session, but this is all about the ECG. It's an audience response system, so we'll be going through several ECGs with panel discussion. Please download the app if you haven't, HRS 2025 mobile app. You go into the Q&A, just that it says Q&A, you go into that, link on the app, and then when the polling comes up, that's where the ARS will be. The polling is anonymous. There's no way to know who said what, but I'd like to have all you all try to poll in. So we have several ECGs. We'll go through several of them, and feel free to use our app to also ask Q&A. We'll be going through those intermittently throughout the talk. So let's get started. Okay, so you can also use your QR cap here, but again, the link on the app should also get you this. So our first tracing, we have a 7-year-old man with newly diagnosed LV systolic dysfunction. Shown here at the top is one part of the halter and the second part is this continuous strip shown below. And the question is what's the mechanism shown here? Your choices are intermittent left bundle with a very long refractory period, AV accessory pathway, fasciculoventricular accessory pathway, vagatonic AV block or blocked APCs. So when the point comes up, I'll give you 15 seconds. And I'll. Excellent, this is what I love about these sessions. So, excellent, so let's unpack this a little bit. I'm going to have Dr. Pinsky go through the slide a little bit. Sergio, this is your ECG. What were you looking for in this ECG? So when one has to read this EKG in the absence, this monitor in the absence of the baseline EKG is more difficult to determine. But what causes attention is that there is sinus rhythm and sinus tachycardia with a relatively short PR and a wide QRS, which is notched in the middle. So one can say this is a left underbranch block. So at night, the patient develops progressive sinus bradycardia, as we see. And eventually, there is emergence of a junctional rhythm. And surprisingly, the QRS becomes narrow during the junctional rhythm. So the answer for this, this is Wolf-Parkinson-White. This is an AV accessory pathway. I don't have the EKG to show, but there is a right anterior accessory pathway that gives an image similar to a left underbranch block. So why is this not a left bundle with a long refractory period? Because if you look when there is sinus bradycardia in the middle strip, the cycle length is much longer than when we have junctional with a narrow QRS. So essentially, if you have a wide QRS with a short PR, and when you have a junctional beat, the QRS becomes narrow. That means that it was an accessory atrioventricular conduction producing the wide QRS. Now, in the past, in the pre-catheter ablation era, when one tried to non-invasively try to determine the refractory period and the risk of an accessory pathway, intermittent pre-excitation was, and it still is, a sign of a pathway with a longer refractory period. But there was always a caveat that you should not call intermittent pre-excitation when the pre-excitation is lost during the junctional beat. That is not reflecting the refractory period of the pathway. So now, this could not be a fasciculoventricular pathway because the fasciculoventricular pathway, the pre-excitation would remain during the junctional rhythm because the insertion of the pathway is below the AV node. Thank you. May I make a comment? Thank you very much. One confusing thing is that this is an old man with LV dysfunction. What do you think about this? I mean, 70 years old with LV dysfunction? Yes. You see a wide QRS, your mind goes somewhere else. Yeah, the first thing one thinks is, of course, this is left boundary branch block. Interestingly, right accessory pathways can produce left ventricular desynchrony similar to a left boundary branch block and reversible LV dysfunction that is cured after the pathway is ablated. This is more common in children. But even in adults, it has been well-described reversible LV dysfunction secondary to a right free wall or antireceptor pathway that mimics a left boundary branch block. And the plan in this patient is we're trying to convince him to come and we're planning to ablate this pathway. Thank you very much. This is a classic finding. I think what he may be getting at in an older patient is structural heart disease. You want to think of when you see a left bundle branch block, think about the possibility of bundle-to-bundle reentry or a right atriofascicular pathway just to complete the loop. OK. Let's get this next one. And we'll discuss this tracing here. So this is a 25-year-old woman, diagnosis of hypertrophic hypermyopathy and a reported history of pre-infectation. Comes with unexplained syncope and daily palpitations. And so this is the ECG here. I'm going to enlarge part of it here. I'll advance it once more, and the question is what is the mechanism? So is this a fascicular ventricular accessory pathway, axillary junctional rhythm, isorhythmic AV dissociation, or is this high-grade AV block? I'll give you guys a few more seconds to look this over, advance, and then we'll pull in. Hypertrophic and reported pre-acidification. So let's see what we got. So let's go ahead and pull in. Give you guys 15 seconds. OK, fantastic. So the majority actually got this correct. This is actually sort of a corollary to the first one. This is indeed a fascicular accessory pathway. And so do you want to go ahead and discuss this, Mel? Dr. Scheinman, do you want to comment on this ECG? I think we basically have, Sergio has very nicely discussed this. So here you have, if you look at the tracings to the end, you can see pre-excitation. You see it best in V3, V4. You see the short PR and a little slurred upstroke. So pre-excitation is present. But lo and behold, when you look to the left and you see these junctional beats, the pre-excitation is the same. So this would be path mnemonic of some kind of a fascicular ventricular pathway. It could be a nodal ventricular pathway as well. You'd need some more data. But this ties in very nicely with the first case that Sergio discussed very well. Yeah, I believe that the thing to think about here is that these don't get updated, but that the history of a 25-year-old with hypertrophic cardiomyopathy, that sort of invokes Dannen syndrome with a LAMP mutation, which is a high instance of sudden death. So she wouldn't die from necessarily this rhythm, but the linking there between Dannen's disease and LAMP is well-described. Just to ask for if anybody in the audience has a question, one question I might have is if you don't know for sure that it's pre-excitation, but think it's a wide QRS, how does this differ from, I probably pronounced this incorrectly, but acrochage, in which you have a sort of independent atrial and ventricular rhythm. It's a form of isorhythmic dissociation. And most characteristically, the PR interval is not constant. It tends to get shorter and shorter and move into the QRS and come out the other side. And then a little while later, it goes back into the QRS and comes out with a normal PR. And I think that is one distinguishing point between this rhythm that we're being presented with and this acrochage thing, which is not all that rare, as it turns out. OK. So much for that. This is not all going to be about accessory pathways, I promise you. OK, our next case. This is a 24-year-old man out of hospital cardiac arrest. He had a loss of consciousness and contention of urine with no jerking movements. He woke quickly and felt normal when he awoke. He's on no medications. There's no family history of sudden death. He was cardioverted and given amiodarone. And shortly after the resuscitation, this is the ECG that you see here. And the choices are, based on what you're seeing here, do you have Brugada syndrome, Long QT syndrome type 3, CPVT, or some combination of A and B, A and C, or B and C? We'll give you a couple more minutes, five seconds, we'll start a run, then we'll advance. Okay. Excellent. The correct answer that we were looking for here was, in fact, combination between Brugada and Long QT3. And I'm going to have Dr. Scheinman send me this tracing. And Mel, do you want to comment on some of the features here that you're seeing? Yes. So this was a remarkable case of a young man, status post-cardiac arrest. And the first EKG, which we didn't show you, was very difficult to discern. But the Brugada pattern was present, as you can see here. So this is taken after he stabilized. And there's two things that are very striking. One is the Brugada pattern. And the other one is the QT interval is very long. As you know, the QT shouldn't be more than half of the RR. And you look at lead 2, for example, the QT is all the way up into the snuggled up to the next P wave. Now, it's hard to be very dogmatic about it when people have sinus tachycardia, as you can see here. But even when the rate slowed down, he still had this feature of a very long QTC, as well as the Brugada. And this is known as the overlap pattern. Do you have any of the other slides? That's the only one we're showing. Okay, yeah, I just wanted to, yeah. So it's, a lot has been learned about the physiology of the overlap because, as was true in this particular patient, he had a mutation in the SCN5A, the sodium channel gene. And it's really interesting. The physiology has actually been worked out. For the Brugada syndrome, as you all know, this is due to the, the SCNA5A abnormality may produce a loss in the peak sodium, which is the beginning of depolarization. However, if you have problems with the inactivation loop, you can have increased sodium pour into the cell, the so-called late sodium current. So you can have a situation where you have an SCN5A genetic mutation, which will give you features of Brugada, as well as long QT. Now, it's well to have this in mind because it has important treatment connections. In the Brugada syndrome, as we know, the drug of choice would be quinidine. But you certainly don't want to use quinidine for somebody with a long QT syndrome. So if you wanted to use drug therapy, your options are to use something like aminophilin, try that. Or in this case, what we did was we adjusted, he underwent insertion of a pacemaker defibrillator, and we increased the atrial rate, and his QT normalized. And he did well for at least the time that we followed him. So these are very rare, but they're very interesting, and they're challenging, both diagnostically and in terms of therapy. Can I make a comment? We have a question from the audience, but I have a similar question. I mean, if this guy came with a cardiac arrest and had a troponin of 10,000, for example, you have ST elevation, you have long QT. How sure are you that this is not acute ischemia? That's my question. The question I have in front of me is, the guy had a cardiac arrest, and he got also amiodarone. How sure are you about the long QT? Yeah, as I say, from the one I showed you, there's some question about being very positive where this is long QT because of the sinus tachycardia. As you know, the QTC is a problem. But even when the heart rate came down, the QT prolonged. This was taken some years ago, and I just don't remember whether we did coronary angiography or not, but we were pretty certain that this was not ischemia. He was a young, healthy person. We might have done coronaries, but I don't remember. Because a long time ago, we had a similar patient who came with a cardiac arrest, and he was transferred to our unit, and he was giving streptokinase at that time. There was no coronary angiography. So that's an interesting point just to point it out. This is basically just regarding the ECG. And also, there's another question, if I may interrupt. Is there a role for maxillitin in this? For maxillitin. Would you prescribe maxillitin? Maxillitin. Maxillitin. I think I would be concerned about use of maxillitin. I don't think there's much of an experience with that in Brugada syndrome. There is an experience using aminophilin. And of course, nowadays, we have the option of ablation for the Brugada if we couldn't control it with drugs. Excellent. Okay. So we have a 75-year-old man with three months of lightheadedness, now with a syncopal episode. This is his ECG before cardioversion. And the question is, what would you recommend now? So your choices are permanent pacemaker, ICD, IV amiodarone, IV procainamide, or coronary angiography. Okay, fantastic. So the answer that we were looking for here is permanent pacemaker. I don't have Mirage do you want to discuss this a little bit? Thank you So the ECG shows heart block with a short long short resulting in TOSAD So on the left hand side of the screen you see P waves sinus P waves at a rate of approximately a hundred You see a wide QRS, which I think is the right bundle pattern You see the QT after that is prolonged to 550 or 600 milliseconds There's a PVC that results in a polymorphic rhythm, which looks like TOSAD with twisting of points So this looks like somebody with Infranodal disease has gone into complete heart block and I say that because of the intrinsic right bundle Prolongation of the QT presumably because of sudden Imposition of a long short sequence and then TOSAD So I think the correct answer here But you didn't share with us the LV function which might determine this choice of implantable device But I think the right answer here of LV function is normal is a permanent pacemaker And this is identical to the very first report of TOSAD by Desserton in about 1935 in an elderly lady who presented with complete heart block, but the Cause of syncope was not bradycardia, but was TOSAD So TOSAD will occur on the imposition of sudden bradycardia and then a PVC will result in TOSAD So I think a permanent pacemaker if LV function is normal is the appropriate choice of therapy Yes Yeah Excellent example. I have a question here, which is similar. Sometimes people who have a complete heart block they have Depressed LV function because of the complete heart block, you know, ejection fraction 40% for example. What would you do in that case? ICD or pacemaker Pacemaker So, why would complete heart block result in LV dysfunction is it the choice is it because of the escape rhythm Yeah, and a topic focus. Yeah Please you know, I have a Comment, you know It's not infrequent that you will see a patient who had syncope and presents to the emergency room And now has complete heart block With a stable escape good hemodynamics. The QT is long so While you make preparations To implant the pacemaker with a temporary wire Whatever. I think it's important to infuse magnesium sulfate in those cases to prevent further attacks of distorsion because more often than not Because of syncope is not Existently and sudden sudden bradycardia and a sisterly but an arrhythmia like this in those patients So it has been my practice for many years to infuse Magnesium while wait while preparing for the pacemaker. I Think it's important to note that it was I think it was Sammy Viscan who pointed out that the patients with bradycardia that develop torsion They will have the long QT. So the ones that are especially Worrisome are the ones that come in with bradycardia Due to AV block or whatever and if the QT is very long, I I think you have to move very quickly Another question from the audience But dr. China, so would you proceed with a pacemaker or an ICD under those circumstances? No, no, no a pacemaker. Yeah Before you take the your final decision, are you going to rule out ischemia with the coronary angiogram? Or you feel you know confident that So it would depend on the clinical history and the risk factors Yeah, but this is not the presentation of somebody with acute ischemia. That's what I would say I So yeah, as dr. Brown was saying this is exactly the way this was first described by desert and back in the 60s This is sort of a Brady induced or sod Okay, let's keep going Okay, this is a 75 year old man With heart failure with reduced gesture fraction. He appears lethargic His pillbox is disorganized and the question is what do you suspect? Among other things. Do you think he took too much beta blocker? Amiodarone the Jackson spirolactone or furosemide When was that that ECG taking I mean what year because the Jackson's is not very good Oh, it's very it's very relevant and in very recent this has taken last night. I'm just having to be trolling for ECGs Okay, let's go ahead and um and weigh in here And we could talk for hours about this and I have talked for hours about this, but we only have a few minutes Okay, so Yes, this is exactly somebody who has ditch excess Dr. Hart, yeah, do you want to go ahead and sort of talk with this? Yeah, I think that's probably one of the most appropriate responses in this situation you can see the underlying rhythm is atrial fibrillation So it's one of the commonest drugs used before for a controlling atrial fibrillation Was digoxin not to maintain any sinus rhythm, but just for rate control you can see the patient that's underlying bradycardia What you can also see is the atrial rhythm sickle fibrillation, but then you can see a dissociative rhythm Basically, he has a heart block with with an escape rhythm going along and frequent PVC's and all of these are Independently described in ditch toxicity. So one of the first thing that comes to mind is the Jackson toxicity in this case The rest of the things beta blocker overdose generally causes profound sinus bradycardia In the presence of a beta blocker, even if you have underlying atrial fibrillation, you probably see a lot of bradycardia Can you have PVC's not really described in beta blocker toxicities? We really cannot explain the entire Clinical picture just based on that alone hypokalemia seems like unlikely which is what you think about and Diuretic overdose or whatever shouldn't be causing this type of clinical picture. So the most appropriate response for this would be Digoxin overdose. Yeah, the commonest with me I also tend to see if not for atrial fibrillation is paroxysmal atrial tachycardia with some degree of AV block Which is the most commonest rhythm described in digoxin toxicity And of course in the setting of hypokalemia, you can also see what you saw in the last EKG you can see presence of polymorphic VT or VF in patients with diogenes toxicity as well Yeah, this is a sample what you described. It's a slow atrial fibrillation regularized Multiform PVC's and some suggestion of the dig effect, which does not imply toxicity whatsoever In my experience. I think that this is part I think it's the most common form of ECG you'll get with dig excess Well, I think the classic description of atrial tachycardia with 201 block or axillary junctional All those are classic and they said sort of describe what dig does I think clinically they're actually much more rare than this Agree, I think most commonly in elderly patients. This is what you see in setting of renal failure basically see them to be extremely verticotic with Multimorphic PVC's I Would just make one comment. These are multi Multimorphic PVC's that late coupled was about 500 600 milliseconds I think when they become early couple that might be a sign of potential EAD activity, which happens with digital toxicity And then the onset of bidirectional VP. I Think other features in the old days We used to see a lot of this and they always used to focus on the QT with ditch toxicity which is actually on the short side and Also, if you look at lead two and three you see that scooped out portion That was also a characteristic of dig and then also Here's somebody with a fib and a kind of a regular rhythm. And so we used to talk about regularization of a fib So all of these were smell like ditch toxicity. I Just want to make one more point that it is Although it's not being used you would see time to time patients coming in on the Jackson It's just something that you always have to keep in the back of the mind Seems like one of the easiest drugs to be used on the outpatient side, you know for a control for a defibrillation So it's always keep that in the back of your mind. I Had that in mind. I mean In the old days in at least in Greece We had the drugs in drops and it was the first thing you would ask a patient Did you have the regular amount of your drops it? No, I didn't feel very well. So I Digested the whole boat, you know, it's You're always gonna have it in concert with ferocibi which will promote hypokalemia You're always gonna have it with a beta blocker. So there's lots of drug drug interactions. This is my Fox Club plant that I grew several years ago I moved to Wisconsin. I took up gardening and You know, this is this is a big victory for me because I've never planned anything before this Fox Club and next to my sinkona Tree for the quinine we fenced in our backyard and the dog started acting really weird And I just like oh, this is gotta be the digoxin plant So that took away the plant and the plant died the dog stayed weird. It's just a weird dog I haven't grown blocks love since Just another fun fact I've talked about digoxin acknowledging before so this is a cane toad Basically, it's actually they some people actually grind these up or Dry them out and they actually put them in their coffee or whatever It's actually a very rare cause of did toxins new patients coming into the ED because the venom gland of this cane toad contains large amounts of cardiac glycosides and this report here of a Case presentation of someone that comes into the ED With this they had toad soup one of them died before arriving in the hospital five patients came in with with constitutional syndromes and then basically they were found to have very large amounts of digital levels and You know the The bufotin toxin produced by the cane toad is it uses an aphrodisiac in a hair store in Japan? And there are certain hosts of these use essence that might like to have some of this in their medicine cabinet so We are all at risk, but I was referring to myself Okay a little more serious now, so we have a 30-year-old woman with structural heart without structural heart disease Who comes in with syncope the numbers are PR intervals shown here? So I'll give you a moment to look at this ECG This is another one from dr. Scheinman And So the question is What is being shown here? Do you have an intranodal mowat's 180 block? intranodal mowat's 180 block intranodal mowat's 2 block intranodal mowat's 2 block Or both intranodal mowat's 1 and mowat's 2 together or intranodal mowat's 1 and mowat's 2 together The PR shown here is 160 milliseconds, and then it gets to 200 milliseconds before the drop QRS Oh, I love the rainbow. Excellent. Good. Let's see, Mel, do you want to? I think you sent me the CCG, but anybody in the panel can weigh in on this. OK, can you go back to the EKG? Now, neither Wenckebach or Mobitz had designations of intranodal versus infranodal. So this is our own construction, or Zach's construction. But the thing to focus on is the definition. Definition of Mobitz 1 AV block is progressive prolongation of the PR interval before the drop beat. So that means you have to have at least two conducted beats in order to fulfill that diagnosis. Mobitz 2, again, you need two conducted beats at the same PR interval and then the drop beat. Now, neither of these designations say anything about the beat that terminates the pause. And in fact, what you see here is very common with Mobitz 2 block. In Mobitz 2 block, with the pause, there is time to facilitate conduction either at the node and or below the node. So the PR interval will frequently get a little shorter. In my experience, it's no more than 40, 50 milliseconds shorter. So the fact that it shortens after the pause doesn't mean anything. It's still Mobitz 2 AV block. This is very important, because you'll see this in patients who come in with an acute MI, who they need pacing straight away. But in any event, that's the important message. Now, in patients with nodal block, when you look at the PR interval that introduces the pause versus the PR interval that terminates it, the change in PR is much larger with the nodal blocks. There you'll see PR changes of 60, 70, 80 milliseconds. But changes of only one small box or other is certainly compatible with Mobitz 2 and with the bundle branch block and left anterior fascicle block. This would put the lesion in the infranodal conducting system. Yeah, I think the lesson that we take from this is I think that just because there is prolongation after the pause, that can easily be a both. Both Mobitz 1 and Mobitz 2 both have that slight prolongation. But again, with Mobitz 2 block, the decrement is much less. And then the fact is the guy has a right bundle branch block and left axis. And so this is much more in line with infranodal disease. In the differential, one has to consider that the first beat is an escape, a junctional escape. But it would be very unlikely that the PR would be the same every time. So if it's escape, you would expect minor differences in that pseudo-PR interval. So being constant, one can say that that beat is conducted and not escape. There are some questions from the audience. Do you have to do an EP study? Or yeah? Yeah. I don't think so. I think the patient went for a pacemaker straight away. OK. And then, could it be both intranodal and infranodal? Could it be both? This is almost for sure infranodal. That's where the disease is. Could be both? Yeah. Because it's very important. You can have Mobitz 1 with bundle branch block that's localized infranodal. You shouldn't think Mobitz 1 is nodal, and Mobitz 2 is infranodal. Mobitz 2, it's either intrahysian or below the his bundle. But Mobitz 1 with bundle branch block, that can be below the his as well. That's very important. In that case, one is a fixed level block, and the other one is a link block. Yeah. Right. Because having two link blocks becomes difficult, right? Because the proximal block protects the distal one from actually, unless you have a fixed right bundle branch block and Mobitz block at the nodal level. So is that a potential mechanism for the third set of grouped beats? PR interval goes from 160 to 200 and stays at 200 without any extension. So is that a possible sign of two levels of block? Yeah. I don't know. I don't think we did the study on this one. But that would be unusual in classic Wankabau. That PR interval would stay steady. Yeah. OK. It's a 12-year-old boy who collapsed after playing tag. And so the question is, what's the cause? Is it a sodium channel mutation, a reanidine mutation, desmosomal plakaphyllum mutation, or elevated serum DIG concentration? And I'll give you a second to look that over and ask chat GPT, and we'll have you guys pull in. Excellent. Excellent. That is the correct response. So who would like to discuss what we see here? Dr. Tendry? So basically, what do you observe in this is basically you see two different morphologies of QRSs, and both seems wide, is it? We're talking about a 10-year-old kid? 12-year-old. 12-year-old kid. And usually 12-year-old kids' QRS complexes are skinny, they're really like spikes. This is pretty wide QRS tachycardia in two different axes, and kind of fulfills the diagnose of bidirectional ventricular tachycardia. If you take the choices that are given, could this be a SCN5A mutation? Generally, SCN5A mutations we're talking about, you know, Bregada syndrome, Long QT syndrome, most of them are associated with ventricular fibrillation as the predominant arrhythmia. And this is not what we are talking about, polymorphic VT, TORSAD, or ventricle fibrillation is what usually you associate that with. The other choice is RAR2. RAR2 classically is very well described to do this bidirectional VT, cataclysmic polymorphic ventricular tachycardia, and this is one of the classic presentations, it's definitely high on the list. If you go down to desmosomal myopathies, placophilin often causes right ventricular dysplasia. Now, they can cause both biventricular myopathies, have scar on both sides, but 12 is too early for a person to manifest a desmosomal-related mutation. And secondly, they usually do not cause bidirectional VT, monomorphic VT. At least in this age group, very fast ventricular flutter, ventricular fibrillation is often the presenting symptom. Last is the digoxin, unlikely that a 12-year-old kid is taking digoxin unless he's been bit by a frog, or that it's growing all these strange flowers in his garden. So I think the most appropriate answer would be an RAR2 mutation. Okay. Yeah, it's of interest, look at V1, this is a, you see a right bundle, a left bundle, so it looks like it's alternating from the ventricles as well as the alternation in the limb leads, so it's bouncing from one ventricle to the other. And just a distinction to digoxin toxicity, bidirectional tachycardia there is usually a narrower complex, because it's coming from the vesicular system. I just want to say this bi-directional is calcium-mediated, that it's common with CPVT as we have, digoxin, and long QT8, Timothy's syndrome, which is again, so that calcium and trigger activity is a common denominator for all these bi-directionals. Thank you. The CCT was during exercise or in regression? He was playing tag, so it found to have CPVT. Okay, this is a 23-year-old man who's asymptomatic. The question is, it's really about what you do next, and I'm hoping there's a rainbow here. So the question is, do you study him, do catheter ablation, observation only, do a treadmill, Holter monitoring, beta blocker therapy, or something else, none of the above? There's the rainbow, okay. Dr. Fisher, what do you think, what would you do in this situation here, in this particular? Well, I think you can, a treadmill is kind of telling you what this does. If the patient is not having delta waves at a rate of 60 or so, chances are that when he gets on the treadmill and gets his heart rate up to 90, they'll disappear. There was a burst of enthusiasm maybe 20 years ago for doing triple testing on people to determine whether they were at risk of sudden death with WPW. That included doing a Holter and seeing if they had constant delta waves or not, and if they didn't, that was supposed to be good. The other one is a treadmill test and see if the delta waves just suddenly disappear, that's good. And finally, giving a medication, either procainamide in this continent or Ashmolen in Europe, and if the delta waves more or less suddenly went out, that was all supposed to be good. So I'm not sure the treadmill testing would add very much to somebody whose delta waves stop at a low rate of 60 to start with. So do you think the treadmill test would add catechol stimulation which might change the characteristics of the pathway? Yeah, it's true that you can give, the alternative is to give a isoprel drip, isoproteranol drip, and see if you can get the heart rate up. You can with certain conditions. People, for example, who have no retrograde conduction, which is a normal variation, you can restore all of them to one retro with an isoprel drip. So that's always a question. But the papers that looked at the value of these three tests tended to include the three tests, the Holter, a treadmill, and a drug infusion. And then the other question is regarding atrial fibrillation because orthodromic tachycardia is not life-threatening usually. And the risk of sudden death in patients with WPW is from atrial fibrillation. So is it worth looking for atrial fibrillation in the old days we used to do that? It's interesting to me, and others may have some experience here, but if you ablate an accessory pathway, people who formerly had a lot of AFib don't have it anymore. There are probably five or six papers out saying that. And of course, five or six other papers that say, well, don't bet your life on it because we have a patient who did have rapidly conducted AFib even though the pathway had been ablated and the patient had a history of AFib. But, and I don't think anybody's ever done the study of just ablating the pathway and not doing a PVI or something. I don't think that's done. I have a question. Does this really tell you anything about the conductive properties of the pathway itself? That there's just this strip? Depending on where the pathway is, what the immunodular conductivity is and change and if there is a facing. Yes, if you have a patient with a very large, particularly left atrium, you can have a pseudo-concealed WPW which is perfectly capable of antegrade conduction, but you don't see it because if you have a very large left atrium and a very lateral accessory pathway, then during sinus rhythm it may not be visible. But on the other hand, if you get your heart rate up, it may suddenly become visible. So that's sort of the inverse of what we're talking about. I think with this EKG, when there is clear disappearance of pre-excitation at the rate of 75, I think one could be pretty sure that the antegrade refractory period of the pathway is not extremely short. And he's unlikely to have very short RR during AFib and he's at very low risk of sudden death. I think that one can conclude from this EKG. Now the question is, if the pathway is in a safe place, why don't go ahead and ablate it, you know, and make the life of this person easier down the road? But, you know, in the pre-ablation era, this was considered a favorably prognostic sign and one would never send a patient like this for WPW surgery, for example. What happens if the patient has an episode? How our attitudes have changed, when we put together the guidelines for supraventricular tachycardia before the last guidelines, the sentiment was exactly what you said, and you said as well. If you see... The most benign thing to see is spontaneous resolution, OK? It's very, very unlikely. There are case reports of people like this who have gone on to sudden death, but it's really very rare. So in our guidelines, we said, if the patient's asymptomatic, you leave them alone unless they had a high-risk occupation or the athletes. The pediatricians, when they have patients with pre-excitation and the kids want to go into athletics, they get very aggressive about it. So in real life, those are the two categories that even though you're pretty sure they'll never have a life-threatening event, you still would intervene, you may intervene. May I ask something which is coming from the audience, but from me as well? Does your attitude towards the treatment of this patient has to do with his job? Yeah, as I said, when we put the guidelines together, it was clear that if you wanted to be a truck driver or a pilot, you had to clean up the EKG. And I remember doing it myself. A kid wanted to go into West Point. They wouldn't let him in. So we cleaned up his EKG, and now he's probably a general or something. Or a shark. Just from the ablation. But then on the specific patient, give me a second, sorry. This looks like an anterior pathway, isn't it? So the chance for having complications in this kind of a patient is higher than if it was a left lateral, for example. So that's my first concern for this patient, to be honest. Hi, Debbie Sherwin from Children's National. I'm an aggressive pediatrician. So we did a study in pediatric patients, and with intermittent pre-excitation, there was still a 10% chance of a high-risk, rapidly-conducting accessory pathway. So the intermittent nature, if it is only at low heart rates, that may be reassuring. But if it's purely intermittent, regardless of heart rates, it's similar to persistent pre-excitation with 10% high-risk. So thank you for sharing that. I think because of the, I mean, all the points that have been made up and that have been made in this discussion, risk stratification from surface ECG used to be a question on the EP boards in the USA, but it's been dropped. Thank you. Well, while people are thinking, I'd like to supplement what Mel said. We certainly have seen patients who have wanted to be, just to expand the list, firemen, policemen, all sorts of jobs, school bus drivers, that they can't do it. It blocks them from employment. And other places will take somebody else first. You're not supposed to do that, but that's what will happen. And so I think it's a real issue of, as you say, cleaning up the EKG. It is probably doing the patient a favor. And I think we owe some of our Italian colleagues the credit for saying, if they have a delta wave or an accessory pathway, just get rid of it. And with respect to the pediatrician viewpoint, George Klein has written a couple of papers now looking at the long-term follow-up of people who had accessory pathways and found that, roughly speaking, a third of them stay the same after a follow-up of 10, 15, 20 years. A third of them get to have a shorter refractory period or are able to conduct faster. And another third of them, it kind of dwindles out and almost goes away. So the variation is huge. And predicting the future is, what did Yogi Berra say? There's a famous saying from Yogi about predicting the future. It's very hard to do. OK. Yeah, I guess you never really are able to rule that out, lower risk or higher. If he was 75, we wouldn't be having this conversation. But certainly, when they're younger, it matters. Mr. Lewis, you want to take over? Yeah, thank you. So you have a 45-year-old healthy woman. And she has these two ECGs taking five minutes apart. 75 minutes. What will the EPS show? I'm not calling on you. You have two traces in sinus rhythm. Who wants to comment on this? All right, they passed the slide for a polling. Sorry? So is this prolonged corrected sinus node recovery time, dual AV nodal physiology, prolonged HP interval, or normal conduction? So you're right. The majority, 86%, right? So who wants to comment on this? So we have two EKGs. The first one has a long and constant PR. The second one has a shorter and constant PR. The QRSs are the same in both EKGs. So this is a manifestation of dual AV nodal pathways in sinus rhythm. One could see different manifestations of this, even an alternating of PR. But this is the most common. A long PR and a short PR. And if you are doing a monitor, you capture how it changes from one to the other. Oftentimes, it's a PVC or a PAC, which makes one of the pathways block, and then the other one shows. I think Charlie Fish wrote the seminar paper on this. Yes? Do you think the vagal tone has to do something with the frequency of the ECGs? Vagal tone has to do something with this? The vagal tone? Do you think that the vagal tone has to do something? The sinus rate is the same. So that's unlikely to be a vagal tone issue. So Dr. Pinsky, I have two questions. In the first ECG, why didn't this initiate AV and RT? And the second question is, why wasn't there double fire? That's interesting, why we don't have double fire. I don't know. Double fire is much rarer. You know, very few patients with dual amyloid pathways have double fire. Why we don't have an echo during the long PR, I don't know. Maybe there is some penetration into the fast pathway and cannot conduct retrograde. That's possible, that there is some concealed penetration. I'll also tell you, this only tells you the antigrade properties of both fast and slow pathways. It doesn't tell you anything about what the retrograde properties are. In general, you would assume that the fast pathway is going to go backwards as well. But that's not always true. You can have antigrade conduction down slow and fast pathway, but could have no PA conduction, meaning retrograde could get a retrograde block. And typically, a determinant of sustaining AV and RT is fast retrograde conduction across the AV node. But there may not be a distal turnaround in any case, so you can't perpetuate reentry. But double fire is also very interesting in the properties regarding what generates double fire. Dr. Scheinman, do you have some thoughts? I think you've published on double fire with this. I think I would favor what Sergio was saying. I mean, that's the conventional wisdom that you have reciprocal concealed, and that's why you don't get. Because Mark Josephson made a big point of that, too, that usually these don't have associated AV and RT. These usually do not. A question from the audience here. The question is, are there factors that leads a preferential pathway that goes down? So the question is, why is it one versus the other? It seems like more of an isotonic issue, but what do you think? I guess the follow-up question here would also be, would you ablate the slow pathways just seeing the CCG? You know, there are some patients like these that when they have the lung PR have symptoms of pulsation in the neck. So that would be a consideration for ablation. Not prophylactically to prevent any arrhythmia, but if there are symptoms during the lung PR, one could consider it. Let's proceed to the next one. So we have a 20-year-old man who came to the ER with palpitations. So you see the CCG. Looks like similar to the previous one we saw. And what do you think? Is it bidirectional VT, pre-excited AF with a posterior septal accessory pathway, pre-excited AF with left lateral pathway, or B and C both? So, the correct answer is D, yeah, it's pre-excited atrial fibrillation with two accessory pathways. This is, let's go back to the tracing. Neeraj, do you want to give a comment? So this shows six ECG leads. The rhythm is irregular, the QRS morphology is irregular. And it's a wide QRS, virtually all the time. In a young patient presenting with this ECG, one would suspect pre-excited atrial fibrillation as the first diagnosis. And then I think the next stage is to identify the accessory pathway location. And even during the widest beats, which signify the largest amount of pre-excitation, the QRS morphology changes. And if we see on the left-handed side of the screen, with the wide QRS, leads two and three are negative. We don't, unfortunately, have V1 on this. But this looks like an inferior location of an accessory pathway. So then as we move on, we see that lead one changes from positive polarity to negative polarity, and the axis becomes inferior, suggesting that there may be a second pathway. So I think this leads us to the conclusion that this is pre-excited atrial fibrillation with two accessory pathways. One is intraceptal, and one is likely left lateral. Thank you. Yeah, it's a, you know, the differential, of course, is so-called pleomorphic ventricular tachycardia, but this is so totally irregular. And also, I agree with Neeraj's point. If you look at the limb leads, it's one form is positive in one and deeply negative, probably negative two, three in AVF, positive AVR. And that is really reflective of a post-receptal pathway. And then the other pathway, look at AVL, see, it's negative. So that's your left lateral. So I would agree that those, even though you don't have V1, you have enough clues. What if I, this is quite an interesting ECG with several different morphologies of QRSs. I think the three ways to the ventricle, at least from what the answer is that they have an X-ray pathway in the right, in the posterior, and also basically, sorry, the left, the posterior, and the AV node itself. So if you look at the last beat, which is different from, there are probably two or three of those beats within there, it looks like there's a fusion as well between the competing X-ray pathways, sometimes making it difficult to exactly localize where the pathways are, as long as they're very discrepant in the limb leads, you're able to say in two different locations. But this is a very interesting ECG. So I think that's why it's wise to look at the widest QRSs and the most pre-excitation for localization. Yeah. Because everything else is fused. Fused. Yeah. So how did you treat the patient? What did you do? Sorry? What did you do for him? We did an ablation for him. Both? Both. It was one of our old cases in the UK. But of course, you can cheat and ask the patient, do you have a 12-lead ECG during sinus rhythm, of course. And also from the history, if he had previously tachycardias or not. And of course, drugs, et cetera. So I think it's very interesting, though, very interesting. So just going back to the prior discussion, do you think the risk of sudden death is higher? That's what I was going to ask. That was my next question. I think we know that people who have two different kind of pathways have a higher chance to get sudden cardiac death. And I think you should be more aggressive with patients like him. Yeah. If you look at this tracing, the shortest pre-excited R to R, when you change the pathway, it's less than 200 milliseconds. It's less than one square. So that clearly puts the patient at higher risk of deteriorating to ventricular fibrillation with this. Yeah. Have you actually seen, in your career, VF degenerating from AF, pre-excited? I'm sorry. I'm sorry. Have you seen a pre-excited AF degenerating to VF in front of you? I've seen it in the lab. I have tracings of that. I never got it in real life. I've seen it once in the ER. And the patient was asymptomatic. And then he went straight to VF. So OK. Let's go to the next one. So you have a 56-year-old asymptomatic woman who came for a regular checkup. And you do this ECG. And you see the rhythm strip here. How do you think? It's sinus rhythm with 2 to 1 AV block, intranodal, junctional rhythm with AV dissociation, sinus rhythm with complete heart block and junctional escape, or sinus bradycardia and hypokalemia with prominent U waves. So, we have again different opinions. My diagnosis is that it's not a 2-to-1 AV block. Usually we ask that in our exams in Greece, Dishon. So you have a trace. If you look into the PR intervals, you see that the PR intervals are varying a little bit. It's not the same PR. And if you wait for a longer rhythm strip, then you would see that these P waves are dissociated from the QRSs. So I would suggest it's an escape rhythm. It's a normal patient. There's no need to have a complete heart block. The QRSs are narrow. And of course, if you see another ECG or ask the patient to exercise or just walk, I'm sure that she's going to regain the normal AV conduction. Any comments? Why is the atrial rate high at rest, about 100? It's 95, you know, yeah. I don't remember. Probably she was anxious. I would have thought I was too wrong with the basic science of arrhythmia, but one comment was too good to be true from the audience, so. Yeah, I mean, only from one trace, you're not 100% sure, of course. But what we did, we asked the patient to walk around and she had the normal AV conduction. So there was no need to do anything more. Okay? Let's go next. So again, we have a young woman who presents with palpitations and a slightly reduced ejection fraction. It's quite common, young adults come to your service and they have palpitations or they have been referred to you. And what is the origin of these PVCs? It's LVOT, RVOT, LV-SAMHIT, mitral annulus, or anterolateral papillary muscle. So yeah, sure. We can go to the PVC panel. Well, I wasn't expecting that amount of spread in this one, but. I think the PVC, I'll just go through how we try to analyze the location of the PVC. As you all see, lead one is negative, right? So all forces are going away from lead one, so it's almost very left-sided. And you can see lead two and lead three are like very tall towers, really very high up. And the fact that lead two and lead three are almost equal tells you it's way up in the outflow tract. Anything, when you start to come down, lead three start to go down in amplitude. And then as you come down to the hiss level, lead three is almost biphasic. So you're really high up. When you're that high up in the outflow tract, the leftmost part of the outflow tract is indeed the RVOT. It's interesting. The RVOT is the leftmost part. But if you start, then fine, that could be the next one would be the left cusp, would be the leftmost part, if you think about where it could have come from. Now, if you then look at the pericardial leads, V1, you can see a sinus beat and a PVC beat. You can see this PVC beat beats the sinus beat. So the sinus beat would be midline. It's beating the sinus beat, so it has to be left of midline, which would automatically place it in the left side of the heart, not on the right side. So you know it comes from the top of the heart, the leftmost side of the heart, and it's got to be on the left side. So the first choice you would pick is the left coronary cusp. Now, could it be coming from aortomotile continuity, right? It's almost, it's on the left side, but it's slightly lower, and also what you would expect to see is a QR pattern in lead V1 that classically tells you it's aortomotile continuity. How about the LV summit? There are sites in the LV summit which are way up, high up anterior. Often you would see more of a left bundle-eyed pattern in the LV summit with a delta wave and then slowly transitioning in, at least in V2, by the time you get to V3, you'll see a more positive, a very similar, but I will not see a very dominant R wave in lead V1. So I think LV-ORT would be the best option here, and mostly coming from the left cusp. Yeah, this will be our last ECG. I think that, this is actually a map to the summit. I think the thing that I was hoping, you did a negative one, negative R, and negative L, it's kind of a triple negative that kind of leads me to think more summit, but I appreciate what you're saying. There's really no way to know sometimes with these, these, these tracings. We're at time. Unfortunately, I asked for a five-hour session and I got a hard no. They gave me 75 minutes. I learned a lot. I just want to thank every panelist here, my co-chair Vassilios. 2025 is the centennial for Eindhoven's building the electric cardiograph, so this was well-timed. Hope you enjoyed it, and I will hopefully see you again next year.

ECG review

Dr. Zach Goldberger

HRS 2025

Wolf-Parkinson-White syndrome

Brugada syndrome

CPVT

accessory pathways

ventricular tachycardia

catheter ablation

interactive Q&A

ECG abnormalities