Hello, this is Frank Marchlinsky from the University of Pennsylvania, and I'm here as part of the core concepts in EP sponsored by the Heart Rhythm Society, addressing the topic of ventricular tachycardia in ischemic and non ischemic cardiomyopathy and also covering core concepts related to unique VT syndromes. Here's a list of disclosures. I'm going to start by providing some background information. We tend to bin ventricular arrhythmias into two broad categories, automatic or triggered focal VTs such as those that originate from the outflow tracts, and occasionally the papillary muscles and some fascicular VTs. These VTs, because they're focal in origin, the ECG becomes very valuable for identifying the focal source of the arrhythmia. Also importantly, if we try to interact with this VT focus, with pacing from a distant site, eventually we'll get to the site and capture it, but we don't really interact per se with the focus like we do with reentrant arrhythmias. We actually capture or overdrive, suppress this arrhythmia, but we don't truly interact with the circuit. And in contrast, we have all the reentrant VT circuits, most scar-related VTs, fascicular VTs, and bundle branch reentrant VTs are binned in this category. And in this setting, the VT ECG indicates the exit from the circuit, doesn't tell us where the best to ablate, but tells us the exit. And we can, with pacing at a distant site, actually begin to interact with the circuit, actually start to spin around like a pinwheel when we pace a little bit faster than the tachycardia cycle length. So we can ultimately create a steady state condition where the orthodromic wavefront from the last beat of pacing will collide with the next wavefront that's coming anadromically from the pacing site, and we'll create a steady state condition with a fused QRS complex from the orthodromic wavefront and the anadromic wavefront. So this QRS fusion is characteristic of this interaction, and we'll talk about this in a little bit more detail, but these are the two major bins. And importantly, when we're thinking about these arrhythmia types clinically, we approach them differently. And for focal VTs, the emphasis is on the 12-lead ECG, and of course, pace mapping and activation mapping information. And in contrast, VTs that are macro-reentrant, particularly those with structural heart disease, the emphasis is going to be on entrainment mapping with additional information gleaned from activation, pace mapping, and the 12-lead ECG. Indeed, the VT ECG is important in patients with structural heart disease. It doesn't tell us where to exactly ablate, but it tells us where the VT circuit tends to exit from the substrate and begin to activate more normal myocardium and generate the QRS complex. So, it creates a starting point for mapping. It also can tell us more about some information about the anticipated substrate, especially for non-ischemic cardiomyopathy patients. So, specifically, we look at leads V1, and looking at right bundle branch block patterns in the setting of coronary artery disease will specifically tell us and suggest an LV-free wall site. Left bundle branch block pattern in coronary disease will suggest a septal origin, typically occasionally from the right ventricle, mostly septal. And then left bundle, especially if you have poor R-wave progression and multiple VT morphologies, might suggest the presence of an arrhythmogenic right ventricular cardiomyopathy, and the ECG provides a clue to that diagnosis. The frontal plane axis tells us whether the VT exit is from the top of the ventricle or the bottom of the ventricles, looking at a superior or inferiorly directed frontal plane axis. And then the precordial leads tells us whether it's basal in origin towards the valvular structures at the base of the heart or the apex. If there's a lot of R-waves across the pericordium, we typically think of a basal origin, and always must consider the possibility that there is a non-ischemic substrate, since it frequently hovers and localizes around the perivalvular region. Something that originates from the apical sites will tend to have early R-wave regression if it's a right bundle, or late R-wave progression if it's a left bundle, and can actually be important clues to the origin of the arrhythmia and important things to think about in non-ischemic cardiomyopathy patients. So here's an example of three ECGs, all of them showing R-waves that are very positive across the pericordial leads. This is in the setting of a patient who was 54 years old with a global decrease in ejection fraction. And in this patient, the idea is that the ECGs can suggest the anticipated origin of the substrate, the very basal QRS pattern with positive R-waves across the pericordium suggests that we may be dealing with a significant perivalvular basal substrate, and we'll have activation proceeding from the base towards the apex, creating these R-waves. And it's always something to think about, particularly in the setting of global dysfunction. In addition, and this is so important, that in patients with non-ischemic cardiomyopathy who actually have a late R-wave transition with a left bundle branch block pattern, we really want to think about a unique arrhythmia syndrome, and that is bundle branch reentry. Bundle branch reentry, of course, spins around the bundle branches, and in the setting, it frequently creates this left bundle branch block superior leftward axis. And as you'll see later on by recording the hiss, we can document the mechanism of this arrhythmia, but should suspect it when we see this left bundle branch block pattern with poor R-wave progression in the setting of a non-ischemic, particularly in the setting of a non-ischemic cardiomyopathy. In addition, when we see multiple left bundle branch block morphologies, frequently with poor R-wave progression across the pericordium, suggesting a more anterior origin. This is common from the right ventricular free wall. Multiple morphologies of VT from the right ventricular free wall suggests that we may be dealing with a very specific anatomic substrate that is arrhythmogenic right ventricular cardiomyopathy. So important ECG clues to get us started with where to map to identify the substrate, and of course where to start mapping to identify the VT circuit and where to ablate. Now a few comments on entrainment techniques and mapping. You had a wonderful lecture by Dr. Stevenson, so I'm not going to detail this. I just want to highlight some clinical applications that I think are important. You know, we use the response to pacing during ventricular tachycardia to help establish the diagnosis of whether it's a reentrant versus a focal trigger to tachycardia. So I just want to review that a little bit more. So it's important to be able to use this clinically and also to help, of course, identify when we're recording from a protected isthmus. So what are the clues from recording during the VT and in response to stimulation or entrainment that suggests that indeed we have an appropriate site to target for ablation. So on this slide, we show you an example of a patient with ventricular tachycardia. It's a right bundle superior leftward axis. And prior to initiating this tachycardia, we see pacing from the right ventricular apex and the QRS, not apex, but the right ventricle, actually more towards the outflow tract region with an inferior axis. And importantly, when we pace just a little bit faster than the tachycardia cycle length and attempt to entrain this tachycardia, we ultimately capture what we believe in this case is a focal arrhythmia and create a QRS morphology during steady state pacing that looks exactly like that of a steady state right ventricular pacing during sinus rhythm. This is consistent with the presence of a focal non-reentrant circuit. And it sometimes, of course, will provide us a clue as to what we need to do to try to map and target the focal site of origin and successfully ablate this arrhythmia. In contrast, in patients with most VTs that are associated with structural heart disease or due to reentry, and in most VTs, when we try to pace a little bit faster than the tachycardia cycle length, we can actually get into the circuit and spin it around like a pinwheel and create the steady state condition where the orthodromic wavefront created by the last pacing complex collides with the next wavefront from the stimulated pacing site, the anadromic wavefront, and we create actually a steady state condition where we have a fused complex being created repetitively during steady state pacing. And, of course, this shows the QRS complex being fused between that of stable ventricular tachycardia and that noted during pacing in sinus rhythm. The QRS complex when pacing at the RV apex has a distinct morphology different than VT, and the pacing at the longer cycle length, but just a little bit faster than the VT, creates this fused complex. When we pace a little bit faster and at a progressively faster rate, we extend this anadromic wavefront so the QRS complex looks a little bit more and more like the right ventricular apical pace complex. And this is referred to as progressive but fixed fusion with faster pacing as we demonstrate entrainment and demonstrate this progressive and fixed fusion characteristic, which typifies a reentrant mechanism. Now, importantly, when we're doing this clinically and practically, you know, it's worthwhile always looking at the pacing in sinus rhythm and noting the QRS complex during ventricular tachycardia. And when we have a complex that looks fused between the two, we just need one pacing complex really to confirm the anticipated high likelihood that we're dealing with, of course, a reentrant mechanism by assessing the QRS during steady state pacing. But progressive fixed fusion with faster pacing rates, less like the VT complex as we get faster, more like the paced QRS complex from the right ventricular apex as we're pacing at a faster rate. Now, importantly, when we're trying to map and ablate ventricular tachycardias, of course, we're trying to identify a site that is ideal for localized ablation to terminate and eliminate the VT. And so we try to develop an understanding of what characterizes the activation and the response to stimulation from a site that's characterized as an isthmus. And this is just a cartoon diagram of a presumed VT circuit. This box in this area shows the isthmus site. And, of course, when we're recording in this isthmus site during ventricular tachycardia, typically the electrogram will be recorded between QRS complexes as activation occurs through the rest of the ventricle, so during electrical diastole. And importantly, when we stimulate from this site, the stim to QRS interval, where we begin to activate the ventricle, will approximate the electrogram to QRS interval during ventricular tachycardia. In addition, when we stop pacing and we look at the return cycle, the stim to the local electrogram at the site of stimulation should equal one full revolution of the VT cycle length. And the post-pacing interval should equal the VT cycle length. So these are the characteristics of an isthmus site and important to be able to recognize the isthmus site for terminating ventricular tachycardia during activation and entrainment mapping process. So here's a typical example, the patient who comes in with a history of a CERC infarct, so has a substrate map with a basal lateral scar. We look at the ECG of the VT, and the VT has a relatively early R-wave progression or regression to negative QRS complexes in V2 through V4, excuse me, V3 through V6, suggesting that this VT is actually exiting from the apical region of this scar. The activation is recorded from this site in mid-diastole, consistent with an area of interest and possibly recording from an isthmus site. Stimulation is performed on the left during this tachycardia, and we see that the stimulation has to follow the same route as the tachycardia, and with the acceleration of the rate to the pacing rate, we see a QRS matching that of the VT, and a stim-to-electrogram-to-QRS interval that is equal to the electrogram-to-QRS interval, and a post-pacing interval that matches the VT cyclin. This is important in this example, this VT was terminated with energy application at this recording site, and we're no longer able to induce ventricular tachycardia. Importantly, it's critical to be able to distinguish isthmus sites from adjacent bystander sites. Now, adjacent bystander sites can mimic isthmus sites because the QRS complex, when you stimulate from these sites, has to exit from the circuit the same way as the VT typically does, exits from the isthmus in the same direction, so create the same QRS complex with pacing. So initially, with evidence of concealed entrainment, you'll think you're in the circuit, but then it's important to look at the intervals, because the stim-to-QRS interval will be a lot longer than the electrogram-to-QRS interval from this adjacent bystander site. In addition, the post-pacing interval will equal the time that it takes to get from the adjacent bystander site to the isthmus, and then travel in one full revolution around the VT circuit, and then return to the stimulation site adjacent to the isthmus. So this will be a lot longer, the post-pacing interval, than the VT cycle length. So there are clues based on the intervals, but you can get fooled if you just look at the QRS complex. So here's an example where we have an isthmus site suggested by the recording of diastolic activation between the QRS complexes during stable VT. However, when we…and we pace during this ventricular tachycardia a little bit faster than the tachycardia cycle length, the QRS still mimics the VT. So we think we may be in an isthmus site. We certainly accelerate the QRSs to the rate of the pacing. However, when we look at the intervals, the stim-to-QRS interval is much longer than the electrogram-to-QRS interval, and the post-pacing interval is much, much longer than the VT…after we stop pacing, is much longer than the VT cycle length. So this is consistent with an adjacent bystander site, and you could ablate for a long time and still not eliminate this ventricular tachycardia. So an important distinction that's worthwhile recognizing. It's also important to recognize some of the rules related to entrainment. You need to have a stable tachycardia. If there's a lot of variability in cycle length, it's really hard to make interval measurements reliably, and it's hard to interpret the results of the response to pacing. You should not pace much faster than the tachycardia cycle length, typically 10 to 40 milliseconds faster than the tachycardia cycle length. If you pace a lot faster, especially if the patient's on a drug therapy, you may see some…have a longer return cycle just due to rate-dependent conduction changes. So, beware, and avoid a high-output pacing if you can to avoid big virtual electrodes that may extend your region of capture. You want to capture very locally, and you need to make sure you capture, because then that is done by making sure your…the QRS complex is accelerated to the rate of the pacing. Remember, typically we can't terminate or change the morphology and still be able to interpret the entrainment response. However, there is a unique clue that helps us identify a probable site that will be effective when you ablate there at terminating the VT. That is, if you see this reproducible termination of VT with infrequently a local electrogram that doesn't propagate with a first beat of a drivetrain or an extra stimulus that's relatively long-coupled, this will suggest that you're probably in a very vulnerable site, and maybe a site that will be very responsive to terminating your VT on a permanent basis with radiofrequency energy application. So termination typically confuses the issue, but this is one setting where it actually provides you with a helpful clue as to where to ablate. So that's stable arrhythmias. Let's now talk about ablating unstable arrhythmias and guiding principles. And we first start off by talking about defining the substrate, the abnormal anatomy that's responsible for the VT, and maybe creating the unstable VT. We do that by looking at both bipolar and unipolar voltage maps, and unipolar especially for identifying mid or epicardial scarring, as we'll talk about a little bit more in a second. Certainly know where to look for abnormal voltage on sinus rhythm ECG, and based on the evidence of an infarct, etc., and of course the patient's history. We also analyze the ECG of VT and recordings that are specifically obtained in the region of the abnormal voltage during sinus rhythm and pacing to help identify surrogates for the VT circuit, specifically surrogates for VT exit sites, as I indicated, the 12-lead ECG of the VT, and pacemap match with a short stem-to-QRS interval that looks like the VT-QRS complex with pacing. And then surrogates for VT isthmus and can consist of either a pacemap match of VT with a long stem-to-QRS, especially as you'll see with sites with dramatic change in pace-QRS complex, and late potentials that occur in sinus rhythm, multi-component split electrograms brought on by pacing, local abnormal ventricular activities, so-called LAVAs, and then channels based on inexcitability voltage and the presence of frequently sequentially activated late potentials. We'll talk a little bit about the importance of smaller and multiple electrodes. We now know that this electrogram and these electrogram recordings with small electrodes can help identify more effectively areas of late potentials and also identify isopronal crowding with delayed activation in sinus rhythm, which again is another marker for VT isthmus. It's important when we're going to talk about all these markers that they haven't been really compared head-to-head fashion in any systematic way, so there's no real head-to-head comparison. Suffice it to say, a lot of these surrogates for the VT isthmus based on recordings in sinus rhythm and with pacing have been targeted effectively to help to eliminate VT. So, here's just an example, bipolar voltage map in a patient with an anterior infarction. Typically, a cutoff of 1.5 millivolts is used. This is based on a study that actually we performed way back when defining normal electrogram amplitude with normal electrograms, 95 percent of them being over 1.62 millivolts in the left ventricle and in the right ventricle, 1.47. So, we typically use a cutoff of 1.5 millivolts to identify the region of normal electrograms and less than 1.5 abnormal electrograms, and quite arbitrarily, because it seemed to be effective in identifying dense scar associated with aneurysm formation, we used a cutoff of 0.5 millivolts to identify the dense scar that's frequently removed from an apical aneurysm, and then the border zone that consists typically of signals between 0.5 and 1.5 millivolts until we reach normal myocardium at the back end of a big apical infarction. Now, because scarring in non-ischemic cardiomyopathies can be a little bit patchy, we tend to move the color range a little bit higher to two millivolts, sometimes even a little bit higher than that, because the scarring can be patchy, but this kind of voltage assessment, bipolar voltage, can give you a view of local myocardium or anticipate what local myocardium looks like and helps identify region of scar and significant VT substrate, which is typical, importantly, perivalvular in location, as we've already mentioned in patients with non-ischemic left and right ventricular cardiomyopathies. Okay, a few comments on pace mapping. So, here's the concept of concealed entrainment and pacing during ventricular tachycardia, where we have unidirectional conduction and mimic the QRS complex of the ventricular tachycardia, referred to as concealed entrainment. So, what we're trying to do with pace mapping is sort of the same concept, and the hope is that by getting too close to areas where we have dramatic slowing of conduction in the VT isthmus, and when we pace, we observe both a long stim to QRS complex, and we have areas that may be more vulnerable to unidirectional block, and we have then unidirectional conduction out through an exit site, which can mimic with long stim to QRS intervals the VT QRS morphology, as shown on this slide. Of course, when there's always the chance that we may not have unidirectional block, depending upon the characteristics of the isthmus and how far away we are from the center of this low area of slowest conduction, and we may end up with some bidirectional conduction. As it turns out, this unidirectional dramatic slowing, at least, if not block, is present in most cases of reentrant ventricular tachycardias that are associated with structural disease in the area of the isthmus, and this was an example of a figure that we got from Rod Tong's manuscript back in 2012, and just shows that when you're pacing in these critical areas of the isthmus, you frequently can get dramatic changes in the QRS morphology with long stim to QRS intervals, and changes frequently from one beat to the next, or with modest changes in output, changes in the wavefront direction. There's wavefront vulnerability at isthmus sites, and helps to help us actually see these characteristic changes with long stim to QRS intervals, and dramatic shifts in the QRS complex that mimic different VT morphologies, and help suggest that we're actually recording from a vulnerable area of the isthmus that demonstrates this wavefront direction alternation and change, and is an appropriate site for targeting for ablation. In fact, Dr. Christian Dichelou has actually sort of, I think, really pushed this concept to another level by demonstrating that he could do actually detailed pace mapping and identify sites that very closely mimic ventricular tachycardia, and as we get closer to an area of the isthmus, a longer stim to QRS interval, of course, and then when at sites where the isthmus is located, when we jump to the other side of the isthmus, we frequently get a dramatic change in the QRS complex, where it's no longer close to the morphology associated with the VT exit, and the original QRS morphology frequently for the ventricular tachycardia, and this represents this jump from one area of dramatic slowing and activation to another area. This is the jumping from the exit of one VT to possibly the exit for another ventricular tachycardia in the other opposite direction we refer to. Of course, it's the entrance site for the first VT, and that site, when paced, will have a very poor match with the QRS exit site, but help us identify, as Christian has suggested, the anticipated isthmus site by creating a line perpendicular to this area. With ablation lesions, one can frequently interrupt the ventricular tachycardia circuit and prevent induction of VT and recurrence of VT, even in patients who have poorly mappable VT. Okay, how about channels? There are a number of ways to identify channels that have been described. Dr. Stephenson, Soejima, and colleagues use this technique, as suggested on this slide, where they identified areas of inexcitability and viable myocardium with excitable tissue between these areas of inexcitability that correlate with VT isthmus sites and can potentially be targeted for ablation. So, pacing and identifying inexcitable areas and excitable areas between those inexcitable areas, and then VT channels by identifying higher amplitude voltage signals in areas of SCAR by adjusting the the color range bar and toggling down to lower values and identifying higher voltage values surrounded by lower voltage values with the higher voltage areas representing a conduction channel and frequently linked to areas where we identified concealed entrainment during detailed VT mapping. So, another method for identifying channels in sinus rhythm, and then late potential mapping, late potentials both in sinus rhythm and with ventricular pacing and even other site pacing can be identified. These channels, these late potentials frequently will activate sequentially through a channel of tissue that is associated with an isthmus site during sustained ventricular tachycardia, and of course these late potentials sometimes can represent dead-end nonspecific pathways, and we pay more attention to them, they're more specific when we pace at the site of these late potentials and mimic the QRS complex with a long stim to QRS interval, and when in sites where there's not only late potentials, but the late potentials are linked to a higher voltage. This was demonstrated nicely combining Matatakis and Gerstenfeld combining the late potential activation with higher voltage channels and increasing the sensitivity and specificity for identifying regions that were associated with isthmus sites during sustained ventricular tachycardia. A few comments on lavas and of course late potentials. Lavas, again, are these abnormal signals that are brought out by pacing emphasized by the group from Bordeaux. There's sort of an offshoot of the late potential idea, sort of paying attention to a lot of other electrogram characteristics that are abnormal. The concept is an important one. Electrograms can become abnormal with alteration of the wavefront, and sometimes these electrogram abnormalities are a clue that you're recording from an isthmus site, and they can be targeted. Of course, it's a bit of a challenge targeting all late potentials and lavas, and of course, again, the rules of engagement, how many pacing sites, how much remapping is required to make this uniformly effective. It can be quite challenging. It's still a work in progress, but it's an important concept that is least worth considering. Also important is the concept of small electrode mapping with multiple electrodes. We begin to see with these small electrodes and multiple electrodes more detailed activation wavefronts that can be recorded in sinus rhythm, and when we see this clustering of late potential activation over a small region and what are referred to as isochronal crowding in sinus rhythm, these sites with the isochronal crowding in sinus rhythm are frequently associated with sites during ventricular tachycardia that are associated with diastolic activation and isthmus sites when you try to do entrainment maneuvers. So, again, the sinus rhythm recordings providing a clue with multi-electrode mapping for where an isthmus is located that can be ablated with minimal actually mapping of the VT, and again, details in sinus rhythm, paying attention to these electrograms to target electrogram features and sites recorded in sinus rhythm to eliminate VT in many patients. A few comments on epicardial substrate. Especially in non-ischemic cardiomyopathy, the epicardial substrate may be greater, of course, than the endocardial substrate. This is particularly true. The prototypic situation is the arrhythmogenic right ventricular cardiomyopathy, where it may have small area of voltage abnormality, typically around the perivalvular region. On the endocardium, more extensive area of voltage abnormality. Because of the presence of fat, that may be quite extensive, and coronaries, there's a lot more attention to electrogram characteristics and not just the voltage. Voltage is a good starting point, but the electrogram characteristics and paying attention to signals that are late and sites where we can stimulate and have pace maps that mimic the ventricular tachycardia and are associated with a long stim to QRS complex. So, well-defined targets for ablation and not just targeting and ablating low voltage areas that occasionally may be due to coronary anatomy and extensive areas of fat. Of course, channels of these late potentials, sometimes even providing more extensive target for ablation on the epicardium, and have been proven to be an important target in selected patients. Now, the epicardium and intermyocardial substrate is really important in non-ischemic cardiomyopathy, and there are several ways to identify and anticipate this substrate that's deeper to the endocardial layers. First and foremost, of course, is imaging. We now use imaging on a routine basis in the laboratory with intercardiac echo, identifying echogenicity at the epicardial substrate in subepicardium in non-ischemic cardiomyopathy patients, aneurysmal formation in arrhythmogenic right ventricular cardiomyopathy patients with MR recordings, and gadolinium enhancement extending to the epicardium. Important clues that we're dealing with in LV epicardial substrate and also unipolar recordings. Unipolar recordings give us a bigger field of view, basically look underneath a viable endocardium to try to identify subepicardium, midmyocardium, and epicardium that may be abnormal. So, using a cutoff of 8.3 millivolts in the left ventricle, 5.5 millivolts in the right ventricle, we've been able to demonstrate when you make endocardial recordings using unipolar signal analysis in patients with normal or near-normal endocardial bipolar voltage maps, you'll frequently identify areas of abnormality that predict the presence of extensive epicardial substrate. With extensive experience and analysis, we of course have learned to use a lower endocardial unipolar cutoff if you're recording through dense scar on the endocardium and not normal myocardium. The endocardium abnormality will attenuate some of the unipolar signals, so you'll need to use a lower cutoff, and actually the reverse is true. If you have thick, viable myocardium with hypertrophy, but looking for a layered epicardial scar, you actually have to use a higher cutoff, typically 9 or 10 millivolt cutoff. Okay, also another clue that you're dealing with epicardial, in this case circuit, will be the ECG criteria. Again, the ECG in structural heart disease tells you about the exit, doesn't tell you the exact circuit, but it's a good starting point for mapping, and we know that VTs that originate from the epicardium away from the Purkinje system in patients with non-ischemic cardiomyopathy and idiopathic VTs have distinct ECG changes, not in ischemic cardiomyopathy patients. It doesn't hold true, there's too much scarring, it gets confusing, but in non-ischemic cardiomyopathy, slurring of the initial upstroke, dramatic slurring, different criteria for that slurring in terms of pseudo-delta waves, intrinsicoid deflection, etc., can be used, and the presence, importantly, since a lot of these scars are basal and basolateral, the presence of Q waves in lead I during ventricular tachycardia are very common for VTs that originate in terms of their exit site from a circuit on the epicardium, and this is from work by Valese from Barcelona when he was with us way back when, but just showing how the presence of this Q wave in lead I really enhances dramatically the sensitivity and specificity for identifying patients who have a suspected epicardial VT circuit in the setting of a non-ischemic cardiomyopathy. It's important to recognize not all the substrate in non-ischemic cardiomyopathy is epicardial, if it's not endo. It may be mid-myocardial, especially basal septal mid-myocardial ventricular substrate and VT origins. These VTs look like they exit right next to the septum, either superiorly and exit and have an inferior axis or from the bottom of the septum and have superior exit, but they typically will look like they're exiting right next to the septum. And you can map the endocardium, the voltage might look normal, the epicardium, low voltage only around areas of fat or at the apex where there's, I mean, fat or coronaries, apex where there's a lot of fat. And it's only by looking at unipolar recordings might you pick up an abnormality that identifies and suggests the presence of an intramural significant substrate that certainly can be picked up by imaging, if done beforehand. And if imaging hasn't been done beforehand, one can also use another trick that is looking at transeptal conduction time, putting one catheter in the back end of the right ventricle, another at the left ventricle, and looking at transeptal conduction time. Normally, it takes 28 milliseconds on average to go from right to left, and it doesn't, it's normal, less than 40 milliseconds. And if you have a delay in activation greater than 40 milliseconds in some patients, you actually have a compartmentalization of the right and left ventricle by the scar. The activation has to go down all the way to the apex from the right ventricular base to cross over from right to left, and then get back to the left ventricular base, sometimes over 100 milliseconds later. So, the mid-septal scar creates this disrupted conduction, we call it compartmentalization of the right and left ventricle, and conduction delay that helps to identify that you're dealing with a septal substrate that may need to be targeted for ablation. A few words on polymorphic VTVF syndromes. And again, it's important to be able to recognize the triggers and the substrate in these unique syndromes. They come in two general flavors. The triggers are frequently from the Purkinje system, either in an idiopathic variety or post-MI in surviving Purkinje fibers. They not uncommonly come from the distal ends of the Purkinje fibers that terminate in the moderator band pap muscle structures. And these triggers actually fire early short-coupled prematures that then trigger ventricular fibrillation. And importantly, we now, since we recognize the link between the distal Purkinje system and the pap muscle and moderator bands structures, we frequently, of course, will use intracardiac echo to confirm catheter positioning on these structures to be able to record activation in sinus rhythm with Purkinje activation, and then triggering sites with early Purkinje activation, triggering ventricular fibrillation, and serving as a target for VF elimination, both idiopathic variety and then peri-infarction surviving Purkinje fibers. And then there's the elimination of the VF substrate. Two common VF substrates have been identified. First, Brugada syndrome, associated with an epicardial RV outflow tract, free wall disrupted myocardium, associated with some fiber disruption and electrogram abnormalities, a well-defined area of electrogram abnormality on the epicardium of the RV outflow tract. These are in patients, same patients who develop ST segment elevation, and ST segment elevation in response to ashmaline, procainamide, flaconide, etc. And this is an area that can get targeted for successful ablation and elimination of this substrate by targeting the epicardium RV outflow tract area of electrogram abnormalities. And then we have J-wave syndromes, initially thought to be a repolarization abnormality. Now we're convinced in most cases it's a depolarization abnormality associated with fibrosis and electrogram abnormalities, typically epicardial inferior basal and occasionally lateral, and the inferior RV and LV associated with electrogram abnormalities that can be targeted again, the substrate targeted and ablated with electrogram abnormality elimination and elimination of the substrate and recurrent ventricular arrhythmias in both of these syndromes. Okay, let's move on to talk about a few other unique arrhythmia syndromes. Bundle branch re-entry that comes in two flavors, one spinning counterclockwise around the Purkinje system and creating a left bundle branch block, left axis deviation, typically the site that triggers the initiation of this arrhythmia as a link associated or in proximity to the right bundle, so you get block retrograde in the right bundle and transeptal activation up the left Purkinje system and down the right bundle, creating a left bundle superior leftward axis, quite typical morphology, spinning around in the opposite direction, either down the anterior fascicle or up the posterior fascicle, creating now a right bundle branch block, depending upon the fascicle used, a different frontal plane axis, but right bundle, left bundle, right bundle pattern typically provoked with left ventricular stimulation, where you get retrograde block on the left Purkinje system and then conduction up the right bundle. So, typically in these patients there is some evidence, though not absolutely necessary, of some baseline conduction abnormalities in complete left bundle, increased HV, not uncommon, though again it can be normal. And how do you diagnose the presence of bundle branch re-entry? Well, if you're really ambitious and you put catheters on both sides of the conduction system in the left and right ventricles, you can actually record from all the components, typical components of the conduction system, the his bundle, the right bundle crossing the septum, and then up the left fascicular system and left bundle to activate again the his bundle region. And this is the circuit for the ventricular tachycardia, and you can record these components, because indeed this is a macro re-entrant mechanism involving the conduction system. Of course, most of us take the easy way out and just record from the his bundle or proximal right bundle region and show that the changes with the initiation of the VT, that his precede the V, and the HH cycle in changes, and with any perturbation with the onset or any perturbation with VPDs, etc., the HH cycle in changes precede the VD. So, this is a Purkinje-driven arrhythmia, not primarily ventricular in origin, it's Purkinje-driven in terms of the circuitry, and this is the way we confirm the presence of this re-entrant circuit involving the Purkinje system. We also can look at the response to atrial entrainment. Atrial entrainment, of course, because we engage the his bundle with atrial pacing, we can get into the Purkinje system and demonstrate with pacing. Sometimes you have to give a little atropine to improve conduction, so you can conduct through the AV node, but with atrial pacing we can actually demonstrate evidence of concealed entrainment, because the conduction will go from the atrium, engage the his Purkinje system, and then the VT circuitry. And in contrast, when stimulating from the ventricle, although at the apex we're close to the circuit, we're actually not in the circuit at the right ventricular apex, and characteristically we see some evidence of manifest fusion. So, here's an example of pacing from the high right atrium during entrainment and cycle length of 290 milliseconds, mimicking the VT QRS morphology, the concealed entrainment pacing from the right ventricular apex. We see some evidence of manifest fusion in terms of the QRS complex compared to the VT QRS complex. Though importantly, the apex is close to the VT circuit, and we use the response in terms of the post-pacing interval to try to determine when we're likely dealing with bundle branch re-entry versus primarily myocardial ventricular tachycardias, and certainly AV nodal re-entry with bundle branch block, right? So, in the setting of bundle branch re-entry, we have a short return cycle that's high probability when stimulating from the apex, because we're near to the circuit, we typically see some manifest fusion. And in contrast, when we pace from other sites for other tachycardias, we look at the post-pacing interval when pacing from the right ventricular apex, and farther away from these circuits that are typically in the left ventricle, we have a longer post-pacing interval. And of course, the longest post-pacing intervals will be recorded up in the AV node with AV nodal re-entry with bundle branch block. So, again, we can use the post-pacing interval to quickly differentiate between the arrhythmia mechanisms and the kind of and location of the VT circuitry, and whether the VT is associated with a circuit that's in the more distant ventricular myocardium due to structural heart disease. So, here's a slide just summarizes the characteristic clues to suggest a re-entrant mechanism associated with his Purkinje bundle branch re-entry. I'll let you just hover over those results. And then a final comment about where we ablate. Now, typically, we ablate and target the right bundle. It's easy to get to, easy to characterize, it's effective, and it will interrupt a circuit that's macro re-entrant. But there are situations where we do want to think about ablating in targeting the left bundle, specifically in selected patients where we have unidirectional left bundle branch block. And this can occur uncommonly, but can occur where in sinus rhythm we see, in this example, conduction retrograde up the left bundle. During bundle branch re-entry, we're conducting retrograde up the left bundle. So, we have unidirectional antigrade block and retrograde up the left bundle. If we give this patient a right bundle branch block, he'll have complete heart block. So, as an alternative strategy, the option of targeting, identifying this left bundle, which is pretty easy to identify in this patient, was easy to target for elimination without causing heart block. Okay. Idiopathic outflow tract VTs. You'll hear a little bit more about this from other lectures. Just want to highlight sort of, again, a core concept and an overview. We typically think about these VTs as being focal or triggered arrhythmias. There's frequently some cyclanth oscillations that are noted. When they form just VPDs, they're typically late coupled. They not uncommonly are associated, of course, with big monophasic R waves when they're in the inferior leads, when they're associated with an outflow tract origin from the top area of the heart. And again, cyclanth oscillation is common. Now, these arrhythmias occur characteristically in the absence of significant structural disease. So, there are exceptions to this rule, but most of them have a normal, therefore, normal voltage map. And this is a distinction that people with patients with structural abnormalities like arrhythmogenic right ventricular cardiomyopathy where they may be having frequent VPDs, multifocal VPDs, multifocal left bundle VTs, and they are associated with a structural abnormality. These VTs that come from the outflow tract are frequently associated with palpitations, hormonal in some, in terms of being triggered with menstrual cycle and just pregnancy, and that they, in women, some women, and important to recognize that because it's sometimes key to sort of when you want a map or where to bring them into the laboratory and how to provoke these arrhythmias with different triggering mechanisms. So, PVC-induced cardiomyopathy is relatively still uncommon, but there is, it can occur, there seems to be a threshold effect, at least 10% PVC burden to trigger these arrhythmias. Rarely do the outflow tract arrhythmias actually come in a short-coupled variety and actually can trigger and have been reported to trigger VF. I think these are relatively uncommon, and more often I've seen PVCs from the outflow tract followed by a PVC from the Purkinje system with a superior axis that is even shorter coupled and causes the VF, but again, just, it's uncommon but may occur. Typically, these VTs that originate from the outflow tract area that are focal in origin are not characteristically initiated by program stimulation, about a third are, that many of them are initiated, though, by burst pacing, and sometimes it's critical to actually do atrial burst pacing to get these arrhythmias to start to fire. Isoproterenol is frequently required at high doses to bring out these arrhythmias and to demonstrate what frequently is pharmacologic provocation of these arrhythmias. Now, when you look at the pharmacologic influences on these arrhythmias, and just the slides summarize these results from Lerman and colleagues, it's clear, or appears to be clear, that the mechanism for these VTs appear to be calcium-dependent triggered activity. You have influence on cyclic AMP metabolism and ultimately alterations in calcium conductance that can result or direct effect on calcium conductance with verapamil, and you look at all these agents, and the best way to interpret mechanistically what is causing these arrhythmias is a calcium-dependent triggered activity, just based on looking at the pharmacologic effects. Now, ideally, these arrhythmias are effectively mapped and ablated. These arrhythmias, because they're focal, have a short or small area that demonstrates pre-QRS activity, typically in the neighborhood of 20 to 40 milliseconds, and it's clear that the ECG provides a lot of clues, as you see, to where to map and how to map. So, it's important, but when you do activation mapping, and it is important that it's important to obviously trigger the arrhythmia. It can be challenging at times. Don't forget to use the 12-lead, like shown on this slide. Use the 12-lead to determine what the onset is so that you're more accurate and hopefully detailed in performing the activation map. We supplement bipolar recordings, looking for a rapid bipolar signal with unipolar signals, the first rapid, largest negative deflection being associated with typical sites of origin, and not uncommonly where we see good bipolar recordings. Pace mapping can be helpful, especially in patients where you can induce the arrhythmia, but you have rare VPDs, and you need to do pace mapping. It's then important to rely on detailed pace mapping, number one, and get template matching that is near perfect. All the notches match typically above, and certainly 90 percent as was first demonstrated in this study, but even better than 95 percent, and we like to get better than 98 percent match to basically target specific sites using pace mapping with a reasonably high degree of success. Certainly, the two are complementary, activation and pace mapping to corroborate the best site and identify the best site for ablation. Now, a little bit of just a few comments on the ECG. I think that this is an important topic because the ECG for focal arrhythmias tells the whole story. It tells you where these arrhythmias are coming from, and importantly, these arrhythmias come from very specific anatomic sites, similar from one patient to the next, so that you can use the ECG to help get a real handle on where to start mapping. And as this slide shows, this is the slide cut section through the RV alpha tract. This is the septal aspect of the alpha tract. There's no true septum. The other side of this is the aortic root, so this is the septal aspect of the RV alpha tract. And typically, most VTs from the alpha tract region, especially younger, healthier people, originate from this septal aspect of the alpha tract and vary from far to the left. We have a numbering system, we use number three, but it's far anterior and leftward, and we're back a little bit more medially on the septum. And when you have an origin from these characteristic typical sites, you typically get a transition, not uncommonly out in V4, big large monophasic R waves in the inferior leads, and then depending upon how leftward it is, you'll even get a more negative QRS complex when it's far to the left, because the outflow tract, of course, wraps around to the left in front of the aortic root, and you'll get a negative QRS complex in lead one. Multiphasic as you move from the more leftward aspect back towards a more medial aspect on the area. This area is typically right adjacent, and most cases probably above the valve. There's fibers that extend above the valve, and that's the targeted area. Now, it's important to recognize that sometimes these arrhythmias originate from sites nearby, not uncommonly from the free wall, and free wall as opposed to septal aspect of the outflow tract will have characteristic ECG features that are important to recognize, because it's from the free wall that tends to be even a later QRS transition, not uncommonly out in V5 or V6 even, and consistent with a sequential activation of the free wall and then the septum, you'll get notching in the inferior leads and smaller amplitude QRS in 2, 3, and AVF, and because it's moving from right underneath lead V2, there's frequently big R waves when your tachycardia originates or VPDs originate from the free wall of the outflow tract back towards the rest of the ventricle. Big R waves in V2 are identified greater than three millivolts, so important features. Now, the lead one will vary depending upon how far to the left it is. If it's more basal and rightward, it'll be positive, and as you move more lateral and typically more anterior, it'll become more negative in lead one. Now, these VPDs and VTs that are idiopathic tend to occur in this almost like an arc that originates from the tricuspid valve annulus all the way to the mitral valve, so let's just talk about some of these other sites specifically. We're talking about, of course, the tricuspid valve region, and the outflow inflow area. We're talking about moving down and to the right, and we get some characteristic ECG changes. So, as we move downward and to the right, we typically get a bigger R wave in lead one, and you compare the R wave in leads two and three, it gets bigger in two than three, and you see now with activation going from right to left a positive deflection in AVL, where typically it's from the top of the outflow tract, it's negative in L and R. So, very characteristic features as you move to the top of the tricuspid valve and down and to the right from the pulmonic valve. It's important that you can distinguish VPDs or VTs that originate from the septal aspect versus the free wall aspect, not by looking at the frontal plane. The frontal plane, again, will show similar pattern in terms of bigger R wave in lead one, two greater than three, big R wave in lead AVL. It doesn't matter whether it's free wall or septum, they tend to be both similar, but when you look at the precordial activation, of course, you're from the free wall, you're closer to all the precordial leads, so you get a later precordial transition, more wider QRS, more QRS notching, and a deeper negative S wave again in V2 and V3. When you're over on the septal aspect, and this sometimes you're going to see an early activation of your R wave, actually positive in V2 and in V3 or significant positivity, and it can be coming from that septal aspect, especially near that parahysian region, and need to beware. So, let's also talk about the ECG features from a little bit more posteriorly in the outflow tract from the aortic cusp area and from the LV epicardium, if we can. This slide just shows you, again, going from anterior to posterior, anterior being the RV outflow tract, free wall, and septal aspect at the pulmonic valve. You tend to have transition in terms of the precordial leads in very late, the free wall earlier in the septal aspect, and then as we move more posteriorly to the aortic cusp region, bigger R waves in V2 and occasionally even in V1, we begin to get some positivity, and by the time we reach the aorta mitral continuity, we begin to see this characteristic QR complex, which is typical of this site that joins the muscle fibers that are surviving at that aorta mitral continuity. So, pretty typical ECG patterns, bigger R waves in V1 and V2, suggesting that there may be more posterior origin consistent with a cusp origin. It's important to identify this left ventricular outflow tract origin. One of the easy ways to do it is to compare the sinus rhythm activation with the VPD or VT activation in terms of the precordial transition. So, if you look at VTs that originate from the RV outflow tract region and you look at the sinus rhythm activation compared to the VT, the VT or VPD QRS complex transitions after that in sinus. So, consistently, and in contrast, when you look at VPDs that originate from the LVOT region compared to sinus, there's an earlier precordial transition in most patients. So, using the comparison of the QRS transition in V2 and V3 sinus rhythm versus the ventricular arrhythmia to help identify a probable right versus left ventricular origin. Other clues exist. I'm not going to go into all the details, but help to identify a probable LV outflow tract origin. Some are, again, important to think about because it's more complex procedure, a little bit more risk that's involved, though not great, but it's important to be able to advise patients based on the ECG features, if possible. Here's another ECG features. This notching in V1 appears to be fairly sensitive and reasonably specific for identifying a site that is not uncommonly at the junction of the right and left coronary cusp, not uncommonly from fibers that extend above the cusp and create late potential activation in sinus rhythm, and with pacing from these sites long to stem to QRS intervals with the QRS complex matching the VT. So, again, ECG features important. It's also, again, important to recognize the use of intracardiac echo, help identify coronary anatomy, help identify anatomic location, especially when working in the cusp region to keep you out of harm's way and help localize these arrhythmias. Just in front of the aortic valve, we talked about the QRS morphology as we move from the hiss region to the aortomitral continuity, and then as you move along the anterior mitral annulus, where some of these VPDs come from, we begin to see a broader QRS complex in lead V1. We transition from this left bundle at the hiss level to over the anterior mitral valve, a right bundle branch block, broad QRS complex in V1, and that's typical of something that's coming from the superior and superior lateral aspects of the mitral annulus. ECG clues that suggest an LV summit origin or associated with the coronary anatomy on the epicardium include delays in activation, initial portion of the QRS complex. This is indexed by an interval called the maximum deflection interval. It measures the time from the onset of the QRS complex to the maximum precordial deflection, the first earliest maximum precordial deflection in any of these precordial leads. Okay, this interval from the onset to this maximum deflection over the total QRS interval, if it's greater than 55 percent, it suggests the possible origin from the epicardium. These morphologic…there are also morphologic clues, like a QS in lead I or a QS in the inferior leads for VPDs from the bottom of the heart and the MCV region, and then finally the V2 pattern break from the LV summit, where we suddenly have an R wave in V1, and then we lose an R wave in V2, and it develops a QS complex and then grows it back in V3, the opposite from the back end of the heart. Some morphologic clues that suggest the presence of LV summit or the posterior LV aspect for the MCV region and LV crux region. Okay, so here's just the important concept. It's difficult to map an ablate epicardial in the LV summit region. We did it a number of times without success. Too many coronaries in the region where these VPDs come from, and it's hard to get your catheter stabilized, and importantly, also this dense fat that marks this area, so it's hard to penetrate through the fat to get these VPDs that have these typical morphologies, an RS, small R, big S in lead one, or QS in lead one, initial QRS slurring, and a V2 pattern break where it's positive in V1, then it becomes more negative, and then much more positive in V3. These are the ECG features. We have a hard time mapping through percutaneous access, and really we've learned that the best way to map these VTs are through the coronary venous system. There are some challenges, of course, and that main challenge being the proximity ultimately to where we find these VPDs and how close we are to the coronaries. Our hope is that we can get at least a half a centimeter away and effectively ablate. If we're less than a half a centimeter, we, in selected patients, think about ablating from some adjacent sites that may be close enough to the area of interest that demonstrates the early activation and still can be ablated safely from the aortic cusp region, RV outflow tract, as far over to the left as you can get, and the endocardium just in front of the aortic root. Again, this is used for situations where the best vein site is adjacent to coronaries, but it sometimes works. You've got to be anatomically close, less than 12 millimeters, but it's an important tip that may be helpful in selected patients when you can't ablate the coronary venous anatomy directly. Finally, idiopathic LVVTs, fascicular tachycardias, come in two flavors depending upon the part of the Purkinje system involved and where the VT, of course, is located and exits, but both of them have the characteristic narrow QRS complex, right bundle branch block morphology. The VT that will be inferior axis will come from the anterior fascicle and will mimic to some extent LV outflow tract, but be much narrower and won't have a big monophasic R wave in the inferior leads. The more common, of course, is the right bundle left superior axis with narrow right bundle branch block morphology superior axis and originating in part from the posterior fascicle. The exact mechanism of these arrhythmias is still, you know, somewhat debated to some extent, but I think there's some consolidation in terms of the general mechanism. It's thought that there's some delayed activation in calcium-dependent peripurkinje fibers, allowing for a region of an abnormality that's in proximity to the Purkinje system where you end up with the potential for a circuit, and that typical circuit will go down a region of delayed activation that's peripurkinje and then retrograde up the fascicular system, and it will not uncommonly show region of delayed activation, not uncommonly in the mid-septal region, and then activation during BT in retrograde fashion where the earlier site is more distal than proximal and in the more well-defined parts of the Purkinje system. That's the typical circuit. There are variations on this theme and quite a few, but I think that's the basic concept. Now, it's important to recognize these are sizable circuits. It's a re-entrant mechanism, sizable circuits. They are, at least in part, calcium-dependent fibers, and these are arrhythmias that can be reset and trained with ventricular exostimuli pacing. You can, if you stimulate from the exact part of the Purkinje system, can actually demonstrate concealed fusion and that show that the conduction system is part of the circuit. You can record diastolic components from over a sizable distance, so it's a fairly sizable circuit, and there's several areas where you can bleed effectively because of the size of the circuit. This circuit is, in part, at least dependent on calcium fibers, dependent fibers, and so they typically terminate with verapamil, and this is an important and unique feature of these arrhythmias. Rarely, these arrhythmias can be focal and automatic, so throw that into the mix, but most of them are re-entrant. They are mapped by detailed activation mapping that, with caution, they can or seem to be superficial and can be bump-eliminated very easily, so there's care and caution in terms of the characteristic mapping. Most, again, are mapped to the inferior septum, starting from the mid-portion, moving a little bit apically, and mapping the anterior basal free wall for right bundle right inferior VT. The activation tries to identify early Purkinje spike when you're mapping the ventricular tachycardia, and, of course, pace mapping can be used. There's limitations. It's not surprising. You can get sometimes pace maps from pacing the Purkinje system where it's perfect and it's ideal and it really is helpful, and other sites that can be confusing or misleading, so it's adjunctive rather than being primary, but I found it to be very helpful. You need to develop a strategy for managing these arrhythmias that get bump-terminated, and I think there have been two strategies that have been reported, and there's a consistency in terms of the anatomic location where these arrhythmias are located based on the information presented from both studies that makes me feel good about the target, and that is in one of the reports by Ouyang, they're targeting the earliest retro Purkinje potentials in sinus rhythm, so this is presumably activation of low-amplitude tissue that typically occurs in the region of the bottom of the mid-septum, and it has variable identification of these signals, but I think that they can potentially be helpful. We've used an anatomic approach with the idea that there's an entrance and an exit, some sizable circuit, and without the goal of causing left posterior fascicular block, indeed fortunately it's rare, we create a small line in the bottom of the mid-septal region, and that has had a significant degree of success. I think if you can find these low-amplitude potentials in the cluster in this area, I mean, it makes sense to target them. This is a pure anatomic approach shown on the left. Both tend to be successful. So, this is just a summary slide. Please look it over. I think we've covered a lot of material, a lot of concepts to pay attention to. I just have two quick questions at the end. Here's to get you prepped for the workshops. The first question is, which of the following tracings is most consistent with SVT with aberration from the four tracings shown, A through D? So, which of the following tracings is most consistent with SVT with aberration? Let's take a look at the correct answer is D. D has a tracing with a very typical left bundle branch block appearance, rapid downstroke of the initial S wave in V1 through V3, an axis that's a little bit leftward, not dramatically inferior in the funnel plane. This is pretty typical left bundle branch block pattern. That's in contrast to the tracing in A, which shows a left bundle branch block pattern relatively rapid downstroke in the precordial leads. But when one looks at the ECG pattern leads 2, 3 in AVF, big monophasic R waves in QS pattern lead 1, this is some variable cyclin activity noted. This is pretty typical of an RV outflow track VT and not characteristic of SVT with aberration. The other two patterns shown are more bizarre looking, more typical for substrate-based ventricular tachycardia and clearly represent ventricular tachycardia associated with an abnormal substrate. So just important rules and concepts. Remember that VT QRS complex doesn't really represent bundle branch block, and there's really a limited number of stereotypical patterns of the Hispokingyi system aberration that can occur. So you see something that looks bizarre, it's more likely to be VT than typical bundle branch block. So it's important to recognize. And then recognize the important rule breakers that have rapid initial activation in healthy hearts. That's the outflow track tachycardias, and of course, vesicular VT that sometimes can mimic a bundle branch block pattern. So important exceptions and important to be able to recognize with pattern recognition and be suspicious of these unique VT morphologies. Okay, last question from the core concepts lecture. 48-year-old man with a history of LAD stent, LVEF of 35%. He undergoes an EP study, planned VT ablation. Three different VTs are shown. These are the 12 leads of the VTs. Which of the four bipolar, RV, and LV voltage maps shown in the panels are most likely to demonstrate this patient's substrate? So here's the four panels. This is a patient who has history of an LAD stent, EF is 35%. Three different VTs, the VT morphologies, frontal plane axis, precordial transition. And here are your voltage maps, so your choices. Okay, this is the correct answer, is choice three. This is a low voltage area on the endocardium in front of the aortic valve and part of the mitral valve. And then a little bit of exaggerated low voltage on the epicardium. Again, this may be fat, but right in front of that same region. This is VT that has three different morphologies, two right bundle, one left bundle, but very early precordial transition for the left bundle to positive QRS complex, all positive across the precordium. These are two very basal VTs. They look like they're hugging and originating from the valve annuli. This is a patient with an EF of 35%. This was a curve ball, the LED stent, no evidence or history of an LED infarct, stented because he had some coronary disease. The EF was depressed. This is a non-ischemic cardiomyopathy. The clues that this was a non-ischemic cardiomyopathy come from the VT morphology. Three VTs that look like they're stuck on the annulus or the upper part of the septum for the left bundle suggest that it's a non-ischemic cardiomyopathy. And here's tracings from an arrhythmogenic right ventricular cardiomyopathy in one, that's not a good match. No left bundle would pour away progression. This is a circ infarct, nothing on the septum. So hard to explain the left bundle morphology with this very basal scar and the circ infarct and LED infarct scar with low voltage at the apex, nothing towards the base. And then the characteristic substrate for patients with a non-ischemic cardiomyopathy, the ECG providing the clue that this patient, three different VT morphologies, all originating from the base, anticipate that there may be a basal substrate, basal septum, basal periannular as the cause, as the basis for this person's arrhythmia. All right, I want to thank you for your attention and I'm going to stop there. Thank you.

cardiac arrhythmias

polymorphic VT/VF syndromes

idiopathic triggers

post-MI triggers

surviving Purkinje fibers

intracardiac echo

catheter positioning

VF substrate elimination

Brugada syndrome

J-wave syndromes

ablation

bundle branch re-entry