Greetings, this is John Miller from Core Concepts in Electrophysiology, representing Indiana University School of Medicine. I want to talk for a few minutes about localization of ventricular tachycardia and PVCs from the 12ADCG. Here are my disclosures. You can see those at your leisure. Dr. Stevenson will be joining in this with some excellent examples of some of these principles here, and he works through just beautifully some of these examples. Now, so why is this important here? We're going to talk about why it's important and how relevant it is, why we need to do this prior to a procedure, some of the general principles of localization of these arrhythmias from the ECG, how that is modulated by the presence or absence of structural heart disease, and some special cases. Also, limitations of these techniques, and finally, a summary before Dr. Stevenson gives those excellent examples. I'm curious about this stuff. Well, knowing the source of where your patient's ventricular ectopy is coming from has several important applications. In pre-procedure planning, do we need to go to the left side? Is this a right-sided procedure? Does the patient need to stay overnight? That kind of stuff. Procedural risks, what to expect? We're going to need to do pericardial access for a variety of reasons here. What is a prognosis? Is the patient going to go away without any problems? Are they going to still have some likelihood of having some ectopy or VT because it's an inaccessible location or very difficult to access safely? Some of the principles used are pretty straightforward stuff in most cases. Generally, the ECG vectors of a standard 12-lead ECG indicate the vicinity of the source, not the exact location in many cases, but at least nailing it down to maybe a quarter-sized area. That's pretty good. If you look at the bundle branch block pattern, left or right, V1 is the best guide for this. Which ventricle does it seem to be the source? If it's a right bundle branch block pattern, it's probably a left ventricular source. If it's left bundle branch block pattern, it's probably, in absence of structural heart disease, a right ventricular source. The presence of structural heart disease, that doesn't go so well. We'll talk about that. Frontal plane axis, another way of looking at things, the inferior leads, probably coming from the top of the heart if it's positive in the inferior leads, coming from the bottom of the heart if it's negative in the inferior leads. Leads one AVL to your right versus left, leads AVR and AVL. Slight shifts from midline, is it more leftwards, is it more rightwards from the septum? Then finally, the precordial R-wave progression pattern, V1 through V6, are they all positive coming from the base, are they all negative coming from the apex? These are pretty good in the absence of significant structural heart disease, but when you throw in scar, hypertrophy patterns, prior surgery, cardiac malpositioning, things get thorny. It's much less reliable in those circumstances. Here's a kind of fluoroscopic views that we might use for electron atomic views. We might use a 60 degree left anterior oblique looking down the barrel, the AV valves, the septum in profile here, apex down here. And then in looking in an REO projection here, looking at the AV valves in profile and the septum on fossil. So if you're coming from the, if V1 is negative, it's coming from V1 sitting over here is coming, going away from the right ventricle, going away from V1. This is typically a right ventricular source. If V1 is positive, it's typically a left ventricular source. Again, these break down quite a bit when you're dealing with structural heart disease, but as a first approximation in the absence of structural heart disease, it's pretty good. Likewise, superior versus inferior axis, superior coming from the bottom of the left ventricle or right ventricle, inferior axis coming from the top of the ventricles, pretty straightforward stuff. Similarly, one in AVL, usually one from a septal source in the left ventricle or right ventricular source, it's positive. And if V1 is negative coming from a lateral left ventricular source with an occasional right ventricular outflow region up here, mainly with negative AV1. Start combining these things or looking at, first looking at basal versus apical comparing V1 or V6. If everything is positive, it's coming from the base. If the majority of the precordial leads are positive, it's coming from the base. Contrary-wise, if V1 is the only thing that's positive and the rest of them are negative, it's probably coming from the apex. All electrograms, all ECG leads in precordial can be negative and looking like it's coming from the apex as well. Some years ago, outflow region and aortic sinus valve salve arrhythmias were evaluated by Dr. Yu Yang and Cook and Company at Humberg. They came up with this uniquely complex structure here of how to analyze these. I'm afraid I cannot remember these things, so I guess there's a map for this more likely, but I can't remember these things. And there's such subtle differences in some of these that I think it's very difficult to say that it's definitely coming from here or there. Nonetheless, it's a rough guideline. This was one of the first attempts to try to do something with these outflow region arrhythmias here. This is a compilation of several different criteria that have been used, a drawing of a certain attitude that I adapted from the McAlpine text. And this is looking down the barrel of the right ventricular outflow tract here with V1 and V2 on opposite sides of the sternum here. The aortic sinuses valve salve is indicated in the right coronary and left coronary osteo with the great cardiac vein and anterior interventricular vein here. So you can look at these and say which seems to fit the best. These are rough guides, slight misplacements of the ECG leads, centered space up or down can make big differences, but they can help you say whether it's endocardial right ventricular, epicardial right ventricular, aortic sinuses valve salve, epicardial LV outflow, epicardial summit. In this region here, the great cardiac vein, anterior interventricular vein or the aortomitral continuity line along here between the aortic valve annulus and anterior leads of the mitral valve. ECG features can help in localization with the lead one configuration, V1, V2 pattern, and the transition point in the precordial leads as indicated in the table here. Again, these are not hard and fast rules, but they're helpful for regionalization. Other dozens of other strategies have been adopted. I'll show you a couple here that have played out reasonably well. This is looking at a complex formula here where you take the R wave in V2 here and divide it by the R plus S during the PVC, the same thing during sinus rhythm. If that number is greater than 0.6, it's likely to be a left ventricular aort. This is a different way of saying the R wave transition. It does a more precise calculation. This is Brian Potensky's work from almost a dozen years ago, 10 years ago. Another group from Dr. Yoshida in Japan showed looking about the transition zone. Each precordial lead is given its own number. V1 is given a number one. If the transition is between V1 and V2, it's one and a half. You take the transition zone of the PVC where that occurs, they are becoming greater than the S minus the transition zone of the sinus rhythm complex and the precordial leads and say, what is that? If that number is less than zero, that indicates left ventricular aort. Generally, these agree reasonably well. Be careful though, because ECG leads are placed in odd places during EP studies because you got the electron atomic mapping patches on, you got the defibrillator patch, people with a relatively small chest, you put the ECG leads where they go, and you end up with some funny positioning. It's best to get these when the ECG is taken in a calm environment, not an emergency room, but in the clinic where people can put the ECG leads on calmly and carefully. Epicardial sources of PVC. This is important to know for procedural planning, especially if you're an individual who doesn't do routine pericardial access for epicardial mapping and ablation. You may need to go somewhere else. If you can figure out beforehand, before you get into a procedure that you can't complete, because that's not part of the things that you do, then you've done yourself your patient a favor by not wasting a procedure on them. Several criteria have been developed in past years. This is Dr. Barroeso's work for a relatively small number of patients. This is a pseudo-delta wave as indicated here. It takes a while for the QRS to start getting going here. Any pericardial lead here, and this is 34 milliseconds in this case, was the cutoff criterion. Delayed intrinsicoid deflection of greater than 85 milliseconds in lead B2 uniquely. This is an example of that. This is 150 milliseconds to get to the peak here. That's pretty long. The duration of the pericardial RS complex in any lead here, that's the shortest onset of QRS to the nadir of the S wave in any pericardial complex. If that's greater than 121 milliseconds, then it's very likely to be an epicardial source. This is all indicators of very delayed propagation, muscle-to-muscle instead of involved in the Hespergindia system. You see that most typically where there is no Hespergindia representation on the epicardial surface. Duration of the QRS complex just overall greater than 200 milliseconds. All of those are indicators or correlates of an epicardial source. Now, none of these have proven useful in post-empath VT, and all of them are extremely sensitive to the effects of nonspecific prolongation of the QRS complex with entry to the McGruggs, sort of channel-blocking drugs. Amiodarone, procainamide, flaconide, papafenone in enough quantities can easily take somebody who doesn't quite meet these criteria into a territory where they do meet these criteria, and you get a false impression of an epicardial source. So here's a couple of examples of this in real life here. I've highlighted V2 because that's one of the ones you're going to be looking at for one of the interval measurements here. So there's a pseudo-delta there that's relatively short. The intrinsicoid in V2, relatively short, shortest RS in the precordial leads, pretty short. Contrary-wise, a long pseudo-delta, delayed intrinsicoid, and the shortest RS being quite long. Okay, so all of these line up just fine. Endocardial origin on the left, epicardial origin on the right, no problem. Problem is, however, that these are exactly wrong. This was actually an epicardial origin after a failed endocardial ablation. Epicardial got it, and this was actually ablated from the endocardium. So these are not hard and fast rules. Both of these were in... One of these was post-infarct... Both of these were post-infarct patients, in fact. Now, I think one factor, one electrocardiographic feature that is immune to the effects of antiretroviral drugs is the delayed maximum peak deflection index. This is from now, 15 years ago, Dr. Wilber's group, and these were idiopathic PT patients with arrhythmias arising from the left ventricular outflow region, but not sinuses and valsalva. So they looked at this and got this maximum deflection index calculation, looking at simultaneous 12 ECGs, looking at the QRS duration from the onset of the earliest to the latest offset of the QRS complex in all 12 leads, and then the time to the maximum deflection is from QRS onset to the maximum positive or negative in each precordial lead, and you take the maximum of that. I'm sorry, the minimum of that. So the shortest time to the maximum deflection in a precordial lead in milliseconds, divide that by the QRS duration. Obviously, this is very sensitive to what you choose as the QRS onset and what you choose as the peak. The peak is usually pretty easy to see, but if you are messed up about the QRS onset or the duration, then you can get a false maximum deflection index. So nothing's perfect, but this was reasonably good. If it's greater than 0.54, 0.55, it's about 100% sensitive and about 99% specific for epicardial origin. I don't find it that useful in my practice because I end up with, on the recording system, you can measure pretty fine points, better than calipers, and these end up being 0.53, 0.55, or is it 0.54? It's difficult. If it's 0.8, that's easy. If it's 0.2, that's easy, but quite often it's hovering around that 0.5 or so. Here's that display here. Now, they had much more scatter than I see in my practice. And here's how the calculation is done here from 2006. Other indicators, so-called newer criteria. This is not so new. It's about 15 years old. This is looking for a Q wave and lead one arising from the superior, typically lateral LV. Doesn't matter whether it's base or apex. Q wave in the inferior leads, where there isn't an infarct, suggest the inferior left ventricular wall as a source. Basal versus apical doesn't matter. Absence of Q waves in the inferior leads should have a little bit of a Q wave with normal propagation. But the absence of any Q waves suggests it's coming from the top of the ventricle and only worked for the base. So this is how this works here, Dr. Mack representation. This is work from Victor Bazan in 2007 for the University of Pennsylvania. Same group, different first author, Dr. Villiers, has looked at pace mapping results in just a bunch of endo and epicardial sites and goes through this algorithm here where their Q waves in the inferior leads know that it must be an epicardial source. Presence of Q waves in inferior leads, QS complexes. The pseudo delta, they found that the maximum deflection index of 0.59 was a better cutoff in their series in the presence of a Q wave and lead one suggesting an epicardial source. Again, very good sensitivity and specificity in not just cardiomyopathy patients, some infarct patients. Now there's some work in people with both infarcts as well as cardiomyopathies, not just normal hearts. This was one of the original pieces. It's now almost 25 years old. This work we did at the University of Pennsylvania, dividing the ventricles into, just again, the aureo and aleo here. So we looked at anterior versus inferior fart, bundle branch block, quadrant of axis, and these eight different airway progression patterns. Most everybody fits into one of these here. And found that it was pretty good. About 93% were correct to within a region that was specified over here. Now, this doesn't mean that that's where you put your catheter in a blade. That means that's where the exit site is. The diastolic corridor is not far away, but it's not exactly right there. And this is amazingly consistent despite every patient having a slightly different portion of their LAD infarcted, different looking sinus rhythm ECG, but a lot of their VTs are just almost superimposable. It's very interesting. Dennis Kuchar from Harvard University came up with a much smaller series and tested with pace mapping. Came with a little different categorization looking at ventricles in three different axes, lateral, central, septal, inferior, middle, and anterior, and apical, middle, and basal. So three different axes. And came up with this algorithm that is a little complicated, but it worked only moderately well, 39% correct. Dr. Siegel from the Mayo Clinic at the time came up with this categorization here. Again, looking at the ventricles from anatomic origins here and saying if it's a right bundle pattern and has positive or negative inferior leads and left bundle patterns are likewise positive or inferior. And you came up with these posterior apical, posterior basal, posterior mid, et cetera, et cetera. This was supposedly 93% correct, but only on a really small number of patients. More recently, Dr. Breuer's group has come up with their own categorization in a relatively large number of cases here. And they looked at two steps. First is finding the limb lead with maximum amplitude, either positive or negative. And then looking at which one of these it seemed to be coming from. This is looking at the American Heart Association 17-point echocardiographic and imaging algorithm with the apex not represented here, 17 is not here. So looking at the maximal QRS amplitude in the limb leads, and then, so AVL would be negative alpha over here, positive alpha over here. Looking at that maximum amplitude and then saying, okay, which of the precordial leads, if they're both, if both the mid-precordial leads are positive B3 and B4, then it's a basal source. If they're both negative, it's an apical source. If they're equivocal, one positive, one negative, it's probably the mid-zone. And their algorithm worked pretty well, 82% correct. I have not found this quite as good and when I try to apply it in my patients, maybe I'm not doing something correctly, but I think I read the paper several times and I think I'm doing it correctly. I just don't find quite the same good results as they do. Now there's some special cases that are worth considering that are somewhat stereotypical. So problematic sites might be such as the papillary muscles. So if you know going into a case, you're gonna be dealing with a probable papillary muscle source. You're in for some headaches, some special tricks needed for consistency of contact in many cases. Here's an example of a posterior, post-remedial papillary muscle source. It has right bottom branch block, leftwards superior axis, pretty typical. But these Q waves in V1 are very indicative of something emanating from within the cavity of the left ventricle. We see these in the posterior papillary muscle and the anterior papillary muscle as well. And in reasonably consistent representation here. So you see those Q waves in V1 and V2 think papillary muscle. Sometimes aerometric continuity, that's the same thing. Left bundle branch block, left axis with this very slow stuttering descent in V1, quite often a lateral basal right ventricle. Tough area to get to and have stable contact. So if you know before the procedure that you're gonna be dealing with something like this. Okay, there's gonna be a slog in there and may have to have deflectible sheets and so on. So there's that sluggish downstroke in V1 over there. This is an example of what just looks like sort of by Gemini, except it's not here. And what's interesting about this is this, most by Gemini, in fact, most PVCs have a fixed coupling of the prior QRS complex. These do not, these are all over the place. It's very short, this is very long over here, this is very long and the QRSs look the same. So these are non-fixed coupled PVCs. Dr. Bradfield at UCLA and our group teamed up with this and found, compiled 73 cases of this. Many were coming from aortic sinuses, valsalva, great carotid vein, interventricular vein, areas that are kind of off by themselves where a focus can fire and not have electrosonic inhibition from surrounding cells, that's one theory anyway. So that's why they can have this variable coupling. Well, they don't seem to be exactly parasystolic, but when you see this gross, crazy variability in coupling interval, we found these to be coming from one of these sites to the aortic sinus valsalva, or papillary muscles can sometimes do this as well. And when there's been a previous extensive ablation that kind of surrounds an area by elsewhere, by a tissue that is not conducting very well, they can have this non-fixed coupling intervals. We also found that syncope, polymorphic VT, and cardiac arrest occurred in an unusual proportion of these individuals. That's an observation, it was not a pre-specified analytical point, but we found that. So that's some cautionary note. The interval that we found was 60 milliseconds or more. So you take 12 consecutive PVCs, look at the coupling interval from the prior QRS complex. If the spread of coupling intervals is more than 60 milliseconds, you're probably dealing with one of these guys here. This is an example of a discordance between leads two and lead three, two inferior leads. Usually they agree, leads two and lead three are not very far from each other electrically on the Eindhoven's triangle, obviously. So they should correspond to each other, but here they're not talking very nicely together. Lead two is positive and three is negative here. And so when two is positive and three is negative, it tends to be a left bumble pattern and right ventricular perihistane or moderator band source. These are worth knowing about because you might endanger the hiss. You might have to do a lot of ablation on a moderator band and close to the apex is somewhat dangerous site sometimes. If lead two is negative and three is positive, quite often it's the interlateral papillary muscle and left ventricle, these are typically right bumble patterns. This is from the 2017 work by University of Pennsylvania. All right, there's some limitations in using these localization methods. Patterns are not exactly predictive and ECG placement is not always consistent, especially if somebody comes in an emergency room, they're very ill, people throw on an ECG, B2 and B3 are backwards or who knows what, limb leads reversed, it gets hairy after a while. So the clinic ECG, when things are quite calm and not necessarily the EP lab, where as I said, the ECG leads can be displaced because of lack of real estate on the chest. We'll say at some sites may have a multiple exit paths leading to very different looking QRS complexes, even though the source is the same, which is quite common in the aortic sciences of El Salva or characteristic of those. Here's an example of that here, where we're pace mapping from the right aortic science of El Salva or the left right junction, I can't remember which, but anyway, we're split by the right ventricular outflow tract. So look at V1 here, it's got on alternate beats, left bundle pattern, right bundle pattern, left, right, left, right, look at lead one, it's flat or all positive, these are crazy things here. So in one sense, it is coming from this left right junction, for instance, the aortic science of El Salva and coursing around the right ventricular outflow tract from left side to right side, that gives a right ventricular last, right bundle pattern. If it's going the other direction around, the right ventricular first, it gives a left bundle type pattern, just as one option here. There've been as many as three different PVCs from one site. Thank you very much for your attention, Dr. Stevenson, we'll pick up things from here. This is the 12 lead EKG localization of PVCs and VT special workshop. I'm Bill Stevenson from Vanderbilt University, and these are my disclosures. So we will go through a series of EKGs, of ventricular arrhythmias, for you to make your assessment as to where these arrhythmias originate. The first is an EKG from a 60-year-old man who's referred for ablation of these PVCs. Ablation at which of the following sites is most likely to eliminate the arrhythmia? And the sites are infraceptal mitral annulus, infralateral mitral annulus, the parahiss region, the inferior papillary muscle, or the infraapical LV septum. You can pause the video and make your selection. So these PVCs come from the infraceptal mitral annulus. So you see that in V1, we have a QS complex with a small terminal R wave, with a then early transition to a large positive R wave in V2. This is reminiscent of the pre-excitation pattern that you see in a posteroceptal accessory pathway. It's consistent with basal septal activation. Now, the frontal plane axis is directed superiorly, and it's much more negative in III than in lead II, and that's consistent with a vector which is pointing up towards the left shoulder. So that also is consistent with early activation of the septum in its inferior aspect. And then across the pericordium, we have dominant R waves, consistent with activation at the base. So this is a PVC focus from the infraceptal basal area, the infraceptal mitral annulus. Case two, this recording is from a 56-year-old man who's referred for ablation of these PVCs. Ablation at which of the following sites is most likely to eliminate the arrhythmia? And again, infraceptal mitral annulus, infralateral mitral annulus, lateral LV papillary muscle, inferior LV papillary muscle, or inferoapical LV. And you can pause the video. Case two, this PVC comes from the inferoapical LV. So it's a right bundle branch block configuration in V1, by which we mean a dominant R wave in V1, putting us in the left ventricle. The frontal plane axis is directed superiorly with large dominant S waves in II, III, and AVF. So we're in the floor of the left ventricle. Now, where are we apex to base? Well, in V4 and V3, we have great big QS complexes, consistent with early activation out near the apex. So this is the inferoapical left ventricle that would need to be depolarized initially to produce this QRS morphology. Case three, a 56-year-old man is referred for ablation of these PVCs. Which of the following sites is most likely going to be the site to eliminate the arrhythmia? Inferoseptal mitral annulus, infralateral mitral annulus, lateral LV papillary muscle, inferior LV papillary muscle, or the inferoapical LV. And you can pause the video, make your selection. So these PVCs come from the lateral LV papillary muscle. So the PVCs have a right bundle branch block configuration. In this case, to clearly see that, you need to look at the rhythm strip that's V1 running across the bottom of the tracing. So right bundle branch block. And then the frontal plane axis is directed kind of horizontally. It's almost isoelectric in AVF and the inferior leads, but rightwards, the dominant S wave in lead one. So that puts us kind of lateral in the left ventricle. And then to get our position in the base to apex region, we look at the precordial leads, and you can see that we have RS complexes in V4, V5, and V6. So that puts us kind of in the mid ventricle. So what structures in the mid lateral LV ventricle? Well, the lateral LV papillary muscle. Papillary muscle PVCs very often have this little initial Q wave in lead V1. Case four. A 43-year-old woman is referred for ablation of the arrhythmia shown. Ablation at which one of the following sites is most likely to be successful? A, the infrared septal mitral annulus. B, the mid LV septal Purkinje region. C, the lateral LV papillary muscle. D, the inferior LV papillary muscle. E, the infrared apical LV. And you can pause the video and make your selection. So these PVCs come from the inferior LV papillary muscle. You can see that they are right bundle branch block in configuration and have a superiorly directed frontal plane axis, so the inferior wall of the left ventricle. And then if we look at the precordial leads, you can see that, again, we have RS complexes in V5 and V6, just a small S wave in V4. so this papillary muscle is probably back closer to the valve annulus. And again, you've got these little initial Q-waves in V1 common with inferior pap muscle and interlateral LV pap muscle PVCs. So the papillary muscles are a common site of origin for PVCs. And although we talk about discrete inferior pap muscle, interlateral pap muscle, often these are complex structures with multiple heads. Very often, the focus originates from towards the tip of the papillary muscle where the cordae insert. And these require careful mapping to assess these. And then the difficulty, of course, is in achieving good stability of your ablation catheter with the papillary muscle for ablation. The precordial patterns can vary a little bit because the papillary muscle may be relatively apical in its location, in which case you can get big S-waves in the mid-precordial leads. Or, as in our last example, it can be relatively basal where you'll have more dominant R-waves across much of the precordium. Case 5. A 24-year-old man with exercise-induced palpitations is referred for ablation of this arrhythmia. Ablation at which of the following sites is most likely to eliminate this tachycardia? The infraceptal mitral annulus, mid-LV septal Purkinje region, lateral LV Purkinje muscle, papillary muscle, rather, the inferior LV papillary muscle, or the infraapical LV. You can pause the video and make your selection. So this is a tachycardia related to reentry involving a portion of the Purkinje system, which very often requires ablation in the mid-septal LV in a region associated with some Purkinje potentials. The tachycardia has a right bundle branch block configuration, so we're in the left ventricle. It has a superiorly directed frontal plane axis, so the inferior aspect of the ventricle, and is mid-cavity in its orientation as assessed from the precordial leads, particularly V3, V4, where we see we have RS-type complexes. It's relatively narrow. The QRS duration is only 120 milliseconds, consistent with involvement of the Purkinje system in this tachycardia. And this is the typical idiopathic interfacicular reentrant VT, or Bellhausen's VT, or verapamil-sensitive VT. This table summarizes for you some of the differences between this tachycardia, the verapamil-sensitive Bellhausen VT, versus papillary muscle arrhythmias, versus arrhythmias that originate from on the mitral annulus. So all of these can produce an arrhythmia that has a right bundle branch block configuration. The frontal plane axis is variable. It can be superior or inferior, depending on the location of the focus. This verapamil-sensitive fascicular VT is almost always sustained, whereas papillary muscle arrhythmias are much more frequent to be PVCs or non-sustained VT, less frequently sustained VT, occasionally repetitive monomorphic VT. The precordial leads are variable, but in general, we'll show an RS configuration in the mid-precordial leads, or at least before, certainly in the verapamil-sensitive fascicular VTs and usually in the papillary muscle VTs. The QRS configuration is typically short for the fascicular-related VT and somewhat longer for the papillary muscle and mitral annular VTs. Any of these can be exercised and induced, but it's really typical of the verapamil-sensitive fascicular VT, less so for the others. This slide summarizes for you some other examples of arrhythmias from these locations. You can pause and study these at your leisure. This flow diagram provides an approach from this nice review article summarized to differentiating electrocardiographically between ventricular arrhythmias from these different origins, the mitral annulus, the LV papillary muscles, or the fascicles. Case six, a 62-year-old man is referred for ablation of the arrhythmia shown. Ablation at which of the following sites is most likely to eliminate the arrhythmia? The infralateral mitral annulus, mid-LV septal Purkinje site, infraroceptal LV, inferior tricuspid annulus, or inferior LV papillary muscle. You can pause, study, and make your selection. So here we see little runs of non-sustained ventricular tachycardia. The QRS complex is left bunduloid in V1, but then with that early transition to a dominant R wave in V2 that's characteristic of a basal septal sort of origin, but then a bit of a pattern break with, again, a dominant S wave in V3. The axis is directed superiorly with QS complexes in V2, V3, and AVF, and leftwards, positive in lead I. So that is consistent with an origin at the infraroceptal area, and that pattern break suggests that it's down a little bit from the very base of the heart. And this is one of a group of tachycardias that we refer to as crux type of PVCs or VTs. These can originate from beneath the septum, anywhere from the base out to close to the apex of the ventricle. You may see early activation recorded from within the middle cardiac vein. They typically have a QS sort of configuration in the inferior leads, consistent with early activation near the epicardium rather than the endocardium, and the QRS in V1 may be left bundyloid or right bundyloid, but then with that variable transition and sometimes a pattern break in the progression of the transition. And these things all point you towards a possible crux region origin for this arrhythmia. Case 7. A 54-year-old man is referred for ablation of these PVCs. Which of the following sites is most likely to be required to eliminate the arrhythmia? A, the lateral mitral annulus, B, the aortic mitral continuity, C, the left ventricular outflow tract, D, the right ventricular outflow tract, or E, the parahysian region. You can pause the video and make your selection. So these PVCs come from the left ventricular outflow tract. So you can see that they have a left bundle branch block-like configuration in V1, and then an RS configuration in V2, where the R wave is relatively broad, although the S wave is still dominant. The frontal plane axis is inferior with tall monophasic R waves in 2, 3, and AVF, and it's inferior and leftward, slightly positive in lead I, and very basal with dominant R waves across the pericordium from V3 to V6. So this is typical of a left ventricular outflow tract origin. This little notched downstroke in V1 is now recognized as being pretty typical of an origin from the commissure between the left and the right sinuses of Valsalva, and just below that in the left ventricular outflow tract, and that's probably among the most common sites of origin for LV outflow tract PVCs. Case 8. A 54-year-old man is referred for ablation of these PVCs. After a prior ablation attempt, a permanent pacemaker was implanted. Ablation at which of the following sites is most likely to eliminate the arrhythmia? A, the lateral mitral annulus, B, the aortic mitral continuity, C, the left ventricular outflow tract, D, the right ventricular outflow tract, E, the parahiss region. You can pause the video and make your selection. So these PVCs come from the parahiss region. So you can see that the PVC has a QR kind of configuration in V1 and then a tall monophasic R-wave in V2, and the PVCs are relatively narrow. They're narrower than his paste beads. And the frontal plane axis is it's positive in 2, negative in 3, so slightly leftwards and in the minus 20 or so range, so almost horizontal, and then very basal with monophasic R-wave in V4, V5, and V6. So this puts you into the parahissian region, and that is consistent with the fact that after a prior attempt at ablation, you wound up meeting a pacemaker. You can see he is pacing here, likely has underlying heart block. Case 9, idiopathic PVCs in a 50-year-old woman are targeted for ablation. Which of the following is likely to be the successful ablation site? A, the great cardiac vein, B, the right sinus of valsalva, C, the left sinus of valsalva, D, the superior mitral annulus, or E, the lateral mitral annulus. So here is the 12-lead EKG from the EP lab showing the PVCs. You can pause the video and make your selection. So these PVCs are likely to come from the great cardiac vein, an epicardial structure. So they have a right bundle branch block configuration, dominant R-waves across the pericordium, so back at the base, and an inferiorly directed frontal plane axis. So consistent with an area of the left ventricular outflow tract, or up at the top of the mitral annulus. Now why do we say the great cardiac vein? Are there features here that suggest this may be epicardial? Well, there is a measure called the maximal deflection index, in which you identify the onset and offset of the QRS complex in all 12 leads, as indicated by the green lines in the PVC at the right, and then identify the earliest peak in the pericordial leads, which is identified by the dashed yellow line, and measure the interval from the onset of the QRS to that earliest peak. And if that exceeds 0.56, so more than 56% of the total QRS duration, that is predictive of early activation at the epicardium. So kind of that slow propagation away from the epicardium. And in this case, even if you just eyeball this, I think you can appreciate that the earliest peak in the pericordial leads occurs well past the halfway point of the QRS duration, and that this is then consistent with possible epicardial origin, and that region of the heart can potentially be accessed from within the great cardiac vein. So in summary, Dr. Miller has a very nice presentation on how to approach the QRS morphology of ventricular arrhythmias. The ECG localization of PVC's NVT is very useful in helping you plan your approach in the electrophysiology laboratory. It's useful in counseling the patient as to what they can expect, what the possible risks and success rate of the procedure is going to be. And it's useful to follow a systematic approach for the ECG localization of these arrhythmias. Realize that in patients without structural heart disease, where conduction through the heart is normal, the ECG is a pretty good guide to the localization of the arrhythmia. It is less reliable when there is structural heart disease, and it can be very misleading when there is severe structural heart disease in areas of scar that modify propagation of activation through the ventricular myocardium. But some patterns of activation are nearly signatures that are useful to recognize and can help make your day in the EP lab short if you learn to interpret the EKG with attention to some of these nuances. Provide you with some nice references and review articles here. Thank you.

ventricular tachycardia

premature ventricular contractions

12-lead ECG

localization

pre-procedure planning

QRS morphology

frontal plane axis

structural heart disease

ablation procedures