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Session III: Invasive Diagnosis and Treatment-6155
Workshop #5: Invasive/Noninvasive Correlation
Workshop #5: Invasive/Noninvasive Correlation
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Hello, this is Frank Marchlinsky from the University of Pennsylvania. I'm happy to be here with you as part of the core concepts in EP faculty and presenting the curriculum that's part of workshop five. These are the questions for some of the questions for workshop five. Here's my list of disclosures. Okay, let's start with our first question. This is case 11. Burst pacing is performed from the RV apex and initiates a wide complex tachycardia shown in panel A. Pacing is then performed from the same site during the induced tachycardia in panel B. What is the most likely arrhythmia mechanism from the choices shown? Focal VT from the parahysian region, bundle branch reentrant ventricular tachycardia, AV nodal reentry with right bundle branch block, and AV accessory pathway mediated tachycardia with right bundle branch block. So these are the four choices. These are the tracings. This is surface ECG recordings at the time of initiation of the wide complex tachycardia in panel tracing 11.1. And then these in tracing 11.2, we have steady state pacing from the RV during the tachycardia in an effort to entrain the arrhythmia. And we see surface ECG characteristics in the middle and intracardiac recordings as noted from the high right atrium, his bundle region, coronary sinus, and from the site of stimulation at the right ventricle on the right. So the question is, what is the best diagnosis from the choices listed? Focal VT from parahysian region, bundle branch reentry, AV nodal reentry with right bundle or accessory pathway mediated tachycardia with the right bundle. Here's the surface ECG tracings and the intracardiac recordings. Okay, here's the correct answer. It's a bundle branch re-entry. Let me walk you through each of the responses that are provided and identify why the correct answer is bundle branch re-entry and not the others. First, it's always good to exclude diagnoses that will show evidence why this is not a focal arrhythmia because of evidence of fixed fusion. We'll exclude the diagnosis of AV nodal re-entry with right bundle by looking at the post pacing interval and noting that it approximates the tachycardia cyclin with only a minor degree of surface CCG fusion. And then finally, we'll distinguish bundle branch re-entry, VT, which is the correct diagnosis from a tachycardia that is mediated by an accessory pathway based on the activation sequence and what's accelerated during entrainment first during whether it's the his or the atrial activation. And we'll walk you through this on the tracings. So, here is the clinical example. This is from tracings 11.1, 11.2, and we see with the initiation of tachycardia with a burst of pacing, the QRS complex during the burst of right ventricular pacing, characteristic ECG features, and then the wide right bundle branch block complex tachycardia pacing, steady state pacing during entrainment shows evidence of fusion. The QRS complex does not look like the pacing that occurred in sinus rhythm that initiated the VT, and obviously looks closer to the ventricular tachycardia than not suggesting that it's probably in reasonable proximity to the circuit, does not match it exactly. So, there's some surface ECG fusion consistent with a reentrant mechanism. This excludes the diagnosis of focal ventricular tachycardia from the his area. This is just a cartoon diagram showing us what we might expect with pacing during the tachycardia from a focal source. Initially, we might see some surface ECG fusion with the onset of pacing, but when we see steady state pacing, the QRS that is generated, that originates from the right ventricle, occurs and the tachycardia is either overridden or terminated, and the QRS complex with steady state pacing should look exactly like that during pacing during sinus rhythm. So, this is what you would normally have anticipated that didn't occur. There was evidence of QRS fusion consistent with a reentrant mechanism and not a focal VT response. And then, focusing on the intracardiac recordings, and specifically, first the post-pacing interval is 280 milliseconds. The tachycardia cyclin was about 260 or 270, excuse me, 266 milliseconds. So, it's pretty close to the tachycardia cyclin, suggesting that it's near to the tachycardia circuit. And importantly, when one looks at the intracardiac recordings in the his region, we see that the hisses are accelerated with the RV pacing, and the last accelerated hiss precedes the last accelerated A, suggesting that, indeed, the hisses are getting activated orthodromically during the pacing, and then subsequently activating the A, and if this were an accessory pathway-mediated tachycardia, that activation sequence would be reversed. You'd get over an accessory pathway and down to the hiss. That's not occurring here. So, this response with a PPI that's just a little bit long, a little bit of surface ECG fusion noted, is consistent with the stimulation from the RV region in proximity to a bundle branch reentrant VT circuit. The his A sequence of activation during the pacing is consistent also with bundle branch reentry, allowing us to establish the diagnosis based on the ECG and the intracardiac tracings of bundle branch reentry. Our next case, case 12, the following history is noted. Following successful PV isolation, the patient demonstrates recurrent AF in response to isoproterenol. All veins remain isolated. The P wave of the first atrial complex triggering atrial fibrillation is shown in tracing 12.1. The intracardiac activation of the same P wave or trigger is demonstrated on multipolar catheters located as shown in the proximal coronary sinus and in the right atrium extending into the superior vena cava. What is the likely origin of the non-pulmonary vein trigger based on the information provided? Superior vena cava, choice A, B, infralateral coronary sinus, C, superior LA posterior wall region, and D, eustachian ridge. So, tracing 12.1 shows the first P wave triggering the subsequent atrial fibrillation. The P wave of note has an inferiorly directed axis, and that excludes the structures from the bottom of the atria, the infralateral coronary sinus, and the eustachian ridge, so now we have either superior vena cava or superior posterior aspect of the posterior wall of the left atrium. And we see the intracardiac recordings show near-simultaneous activation of the catheter in the coronary sinus, and instead of the coronary sinus being activated sequentially, it's activated actually simultaneously. All the electrodes are getting activated near the same time, as is the timing of the activation to the crista. This suggests a source between the crista and the coronary sinus, and is consistent with a source from the posterior wall of the left atrium. Here's a detailed description of the individual possible responses, and why some are correct or incorrect. Again, the correct answer is superior posterior LA between the isolated pulmonary veins. This is just a schema for how you identify the origin of this trigger based on the P-wave in the intracardiac electrograms. In this case, the trigger appears to be from the superior aspect of the posterior wall. Inferiorly directed P-wave that's positive across all the pericordium, consistent with a high posterior origin. The question is, is right or left atrium, where is it located? And then the intracardiacs highlighting this simultaneous activation from this posterior wall source with simultaneous activation to the right atrial catheter and the left atrial recording from the proximal coronary sinus. This simultaneous activation is a tip-off that we have a source that's between the two multipolar electrode catheters consistent with a posterior wall origin, identified again by the ECG information and the intracardiac recordings. This was treated by extending the isolation to include this focal source on the posterior wall with elimination of the trigger in response to additional isoproteranol. This slide just shows you the example of what to expect when you have a recording of activity from a trigger that originates from the superior vena cava. If a catheter is placed into the right atrium and extends up into the SVC, as shown on this fluoroscopic image and this cartoon diagram, typically in sinus rhythm, the second electrode or third electrode pair that's located at the junction of the SVC and the right atrium will be activated earliest. With the onset of the trigger that initiates AFib, the APD originates from the SVC in this case, so the activation changes. So now the distal electrode of this multipolar catheter that extends into the SVC is activated earliest. So, intracardiac electrogram information providing clues to the diagnosis of the source of triggers. Here's case 13. It shows a sinus rhythm 12-lead ECG and some additional electrocardiographic features that are important to recognize on this tracing. And this is the 12-lead ECG for this patient, who's a 60-year-old man with persistent palpitations, and he experiences the palpitation at the time this tracing is recorded. So, the arrhythmia correlates with the symptoms. A 24-hour holter quantified a PVC burden at 18%, and the patient is interested in pursuing catheter ablation. So, based on the ECG assessment of the arrhythmia, which statement is most likely to be true related to the mapping and ablation of the patient's PVC? And the PVC will probably be eliminated by mapping and ablation of A, the LV summit by the epicardio-coronary venous system, B, the LV epicardium directly via a percutaneous approach, C, the right coronary cusp, D, the posterior aspect of the right ventricular outflow tract free wall. Those are the four choices. Here is the arrhythmia shown in the tracing. Here's the answer to the question. The correct answer is C, the right coronary cusp. The other answers are incorrect. The LV summit by the epicardio-coronary venous system. Typically, as you'll see, as a negative QRS complex in lead one, a pattern break in V2 that goes from positive in V1 to more negative in V2 before becoming positive again in V3, and a delayed upstroke typically in the initial activation of the QRS complex. It's important to recognize that LV epicardial approach in the very base of the heart, in the superior aspect of the summit, rarely is effective. There's too much fat and coronaries that preclude a direct epi ablation in most patients. Only when it's a little bit more lateral and leftward away from the fat and coronaries can it work, and the ECG is typically then more negative in lead one, shows delayed initial activation, frequently has actually a right bundle branch block pattern. And finally, D is incorrect, the RV alpha tract. Typically, the alpha tract shows a later precordial transition. Here's a detailed discussion. I'm not going to go over it with you, but it highlights again in even more detail the key features that allow you to make the appropriate diagnosis based on the ECG assessment. And then to highlight and to emphasize these ECG features, just some ECG tracings. This was the right coronary cusp VPD, the clinical example. And then this just shows the data that's been emphasized for the right coronary cusp VPDs, typically being positive in lead one as it moves from right towards the left aspect of the ventricle in the right coronary cusp, tends to be more positive in two than three, though sometimes marginally so. Again, moving from right to left, and then has in the precordial leads, although a left bundle branch block is typical in V1, there is an early precordial transition. So, it tends to certainly be positive by V2 and frequently has significant, excuse me, V3. It's positive, tends to have positive components in V2 in most examples. So, that's that right coronary cusp. And just to show you the VPDs that have been reported to be ablated from the LV epicardium by a direct percutaneous approach in the outflow tract region tend to be more lateral, more negative in lead one, and frequently have a right bundle branch block pattern. And because they're associated with epicardial origin, not uncommonly there's even more dramatic initial slurring of the QRS complex that suggests an epicardial origin away from the hisperkinesis system. And then finally, the 12-lead ECG from the RV outflow tract free wall, very late R wave progression. Here's additional references for you to refer to. Here's case 14. Which of the following is true based on the information shown during the spontaneous termination of a wide complex tachycardia and then stimulation during the same tachycardia from the left ventricle, the site indicated on the x-ray images. The site is the same in tracing 14.1 and during the pacing as shown in 14.3, the catheter remains in the same position. And the choices given include the site of stimulation is from a bystander site adjacent to an anatomically protected VT isthmus. There is evidence of entrainment with concealed fusion when stimulating from a component of the VT circuit on these tracings. There's evidence of concealed accessory pathway mediated tachycardia. The arrhythmia is VT with a left bundle branch block morphology and probably originates from the right ventricle based on the entrainment response. So, these are the choices. These are the tracings. This is the surface ECG tracing showing all 12 leads and then intercardiac recordings from the high right atrium, the left ventricle in the anatomic position shown with the recordings demonstrated during the tachycardia, and then when the tachycardia terminates, and then recordings from the right ventricular catheter. And two right ventricular catheters, one placed proximally, and then one placed more towards an apical site. This is the catheter position in the REO and LAO image, and then tracing 14-3 demonstrates the response to LV pacing from the site as indicated by the arrow. It's the same site that was recorded during spontaneous termination. So, it's obvious that this site of stimulation is from the proximal Purkinje system in the left ventricle. And importantly, during this stimulation, this stimulation shows a left bundle branch block QRS pattern. And during this stimulation, the tachycardia is accelerated to the rate of pacing. There's a long stem-to-electrogram interval that approximates, excuse me, QRS interval that approximates the electrogram-to-QRS interval. The return cycle equals the tachycardia cycle length and is not delayed. So, this suggests that we're actually stimulating from the Purkinje system on the left and are in the circuit. Simultaneously, we see from recordings this patient that we ended up with, the evidence during the left bundle branch block wide-complex tachycardia of a right bundle potential preceding the QRS complex, and that evidence consistent with this being bundle branch reentry. So, in this example, we have entrainment with concealed fusion and stimulating from a component of the VT circuit. The circuit with bundle branch reentry involves both the right and left conduction system. So, you can actually stimulate and, in selected cases, capture just the left Purkinje system, especially if you're using low output pacing, and entrain from that Purkinje system, demonstrate concealed entrainment with an appropriate response consistent with bundle branch reentry and ventricular tachycardia. This just shows you the intervals that were measured and approximated for the electrogram to QRS and the return cycle and the VT cycle, and suggesting that, indeed, this is concealed entrainment from a site within the tachycardia circuit and shows the suggested route of the circuit down the right bundle and up the left bundle. Retrograde the left bundle is evident in terms of the activation when the tachycardia terminates. Importantly, this is not a V reentry. The A's are dissociated from the V's. This is a typical bundle branch reentrant pattern with stimulation from the left ventricle or fascicular system and demonstration of concealed entrainment. It's an example, in this case, of left bundle, bundle branch reentry, and, importantly, you can get the circuit to spin around in a clockwise direction and get right bundles, especially if you stimulate from the left ventricle. And a schema for that pattern of activation when you have left bundle branch block with bundle branch reentry or right bundle branch block. Okay. Next case 15, 56-year-old woman presents with generalized weakness and palpitations. Which of the following diagnosis of best applies to the ECG tracing shown from the choices listed? Electrical alternans due to late coupled ventricular bigeminy with fusion, electrical alternans due to pericardial effusion, electrical alternans with an atrial tachycardia, electrical alternans due to two-to-one conduction over the notofacicular accessory pathway. So electrical alternans speak to be changes in the QRS complex of noted. What's the basis for it from the four choices listed? Late coupled bigeminy, pericardial effusion, atrial tachycardia, or two-to-one conduction over a notofacicular pathway. Here's the tracing just blown up for you to review. Again, electrical alternans is present. What's the most likely cause of the electrical alternans? The correct answer is B. The patient has a triad of sinus tachycardia, the electrical alternans, and the QRS voltage during the electrical alternans is fairly consistent. The B-to-B shifts with a QRS amplitude less than 10 millivolts, consistent with a likely presence of a pericardial effusion. This was a fusion that was evident and present during echocardiographic assessment, pretty dramatic. Other causes of electrical alternans include severe LB dysfunction or myocardial ischemia. The other answers are wrong. There's no evidence of late coupled but ventricular bigeminy. The width of the QRS complex does not change significantly, even through dramatic changes in the amplitude of the QRS complex. That makes the presence of fixed coupled ventricular bigeminy highly unlikely. Alternans with atrial tachycardia never occurs unless the rate is incredibly fast. It's really uncommon with slower rates greater than 150 or less than 150 beats per minute, 400 millisecond cycle length, and two-to-one conduction over a fasciculoventricular pathway. As you'll see, the PR interval remains constant, so there's really no evidence of alternating conduction over a fasciculoventricular pathway. Here's what you would see if you had a fasciculoventricular pathway with B-to-B alternans. You would see alternating PR interval, because the beats that conduct over this importantly pathway that's not associated with any arrhythmias but does produce some shortening in your HV interval when you conduct over this pathway have a typical pattern, the short PR interval, the QRS width that's a little bit wide but not too wide as part of that ventricle gets activated early. Typically, this is a pathway that dumps into the proximal septum and creates an earlier precordial transition in V2 and V3 characteristically. Again, the HV tends to be short but not negative. So, these are the characteristic features. Again, in this case, for the alternans, you would have seen B-to-B changes with short PR interval in the alternating beats, and we did not see that PR interval was constant. This slide just shows you an example of rapid SVT and the typical alternans pattern that one sees when you have very rapid tachycardia. In this case, there was sinus tachycardia but not a very rapid rate, super rapid, and this is a typical for just a rate-dependent change that you see with SVT. Okay, case 16, entral PV isolation is performed with a lesion set as shown in the image, 16-1. Adenosine is then administered by recording from the ablation catheter, with the ablation catheter placed in the left superior pulmonary vein and the CS catheter, excuse me, and that circular mapping catheter in the left inferior pulmonary vein. So, a lasso catheter in the left inferior pulmonary vein, ablation catheter left superior pulmonary vein, and a CS catheter is placed with poles 1, 2 being the distal recording electrodes. And you'll see the tracings recorded in sinus rhythm and during left superior pulmonary vein pacing with the administration of during the administration of adenosine. So, here's the tracings just for you to look at. This is the sinus rhythm recording in response to adenosine, and then quickly pacing was performed from the ablation catheter that was placed in the left superior pulmonary vein. In the left superior pulmonary vein. So, the question is, from the tracings shown following the administration of adenosine, there's evidence of entrance into and exit out of the left pulmonary veins. There is conduction into the left inferior, but not the left superior pulmonary vein. There's exit from the left superior pulmonary vein directly to the left atrium. There's conduction from the left inferior pulmonary vein to the surrounding left atrium observed in sinus rhythm and with left superior pulmonary vein pacing. Okay, so let's just review these tracings. The tracing on the left, again, is sinus rhythm tracing after administration of adenosine. See some PR prolongation, slowing, and the rate administration of adenosine is evident, and one sees, in this case, the presence of isolated firing burst in a catheter that was positioned in the left superior vein, and it's noted, and then conducts to the left inferior pulmonary vein, but this beat doesn't conduct out of the veins. We have dissociated sinus rhythm here on the initial part of the tracing, and then the last beat, we see the same pulmonary vein firing in the left superior pulmonary vein. It conducts to the left inferior pulmonary vein, and then reaches the left atrium as we see a shift in the activation pattern from proximal to distal, sinus rhythm to distal to proximal as activation comes out of this left inferior pulmonary vein. When we paste, we confirm this exit out of the pulmonary vein with the administration of adenosine. This is left superior pulmonary vein pacing. Conduction is then moves to the left inferior pulmonary vein, and then activation proceeds distal to proximal in the CS from the left inferior pulmonary vein. So, the correct answer is D. There is conduction from the left inferior pulmonary vein to the surrounding left atrium observed in sinus rhythm and left superior pulmonary vein pacing following the administration of adenosine. The rest of the answers are incorrect. This is just a schema with the arrow shown highlighting the pattern of activation in sinus rhythm at the end of the tracing out of the pulmonary veins and with left superior pulmonary vein pacing following the administration of adenosine. Okay, our last case, 56-year-old man with recurrent VF. This is case 17. 56-year-old man with recurrent VF, seven days after acute myocardial infarction. This is the recurrent VF episodes shown on tracing 17-1 episode occurring in the baseline state following the administration of IV procainamide and following IV amiodarone. Based on the ECG recordings, the question is which of the following is most likely to be true. The patient has probable drug-induced long QT syndrome and should undergo pacing therapy to prevent additional VF. The patient has recurrent coronary vasospasm triggering VF and should be treated with diltiazem. Ablation that eliminates VF will likely target the Purkinje system and the coronary angioplasty or coronary artery bypass grafting is needed to stop recurrent VF. This is the most likely to be true. The correct answer is C, ablation that eliminates VF will likely target the Purkinje system. It's important to recognize that this is a common arrhythmias syndrome that is surviving Purkinje fibers that occur in the setting of a fairly typically sizable infarction, create the source of short-coupled, shorter-coupled, not uncommonly PVCs, they're not always short-coupled, but PVCs that have a relatively narrow QRS complex, and this is lead II that's being monitored, the superior QRS axis relatively narrow, triggering in patients with non-uncommonly recent infarction recurrent episodes of ventricular fibrillation. It's important to recognize that this Purkinje firing creates PVCs that can be targeted for ablation, effectively mapped and ablated. The patient obviously doesn't have evidence of QT prolongation. There's no evidence of preceding ST segment shifts consistent with coronary spasm, and although obviously in the patient with coronary disease one might worry about with recurrent VT, VF, the ongoing ischemia, there's no evidence suggestive of acute ischemia precipitating these episodes, and this is less likely than choice C. So, choice D, that this is all ischemic-related, less likely than choice C, where we have a typical Purkinje-like trigger with a relatively narrow PVC firing in the post-infarction patient triggering VF. This is the intracardiac recordings from the patient showing the Purkinje activation in sinus rhythm and with the PVC that was targeted. This is the edge of a fairly sizable anterior antereceptal infarction, superiorly directed P wave, so mapping the Purkinje system inferiorly identified this trigger that was targeted for ablation, eliminating the potential to have recurrent VF in this patient as the primary trigger for this recurrent life-threatening arrhythmia scenario. Okay, thank you for your attention, and I hope you enjoy the rest of the Core Concepts curriculum. Hi, this is Greg Michaud from Vanderbilt University Medical Center in Nashville. Welcome to Core Concepts in EP and BoardPREP Workshop 5. The first case shows an episode of SVT termination in a telemetry strip. The middle lead approximates V1. Based on your observations, which mechanism is most likely? Atrial tachycardia, ORT utilizing a right free wall accessory pathway, ORT utilizing a left free wall accessory pathway, typical AVNRT, atypical AVNRT. Here's the figure. I'll pause for a minute so you have a chance to look this over. Take out calipers as you need to. And I think the best answer is ORT utilizing the left free wall accessory pathway. So how in the world can you diagnose that from a telemetry strip? Well, a lot of it has to do with looking for the same things we look for in EP studies, where we purposely put in PVCs, but nature may also provide us with the same answer. And here's an explanation for that, but let's talk about it with the tracing in front of us. So here we can see a tachycardia. The QRS morphology is the same as during sinus rhythm. This QRS and that QRS, sinus rhythm, PQRS, PQRS, PQRS, tachycardia over here. We can see P waves. This part of the T wave does not have this hump and bump. So that's a P wave. It's not as easy to see in the others, but you can clearly see it in this V leaf. And what do we notice? There's a PVC that occurs at the end of the tracing. All these A's are on time. What's early is, and slightly early in changing morphology, is this QRS. So this would indicate there's fusion between the native QRS and this. We also notice that it has sort of a right bundle morphology. So it must be from the left ventricle. So we have a left ventricular PVC. It fuses with sinus rhythm. We know that because it barely changes the QRS, but enough to see the difference. And it blocks retrograde. So what can we say? We can say it's not AT. This PVC didn't conduct up to the atrium prematurely and stopped AT. So this can't be AT. This can't be AVNRT because the PVC is fused. It wouldn't be expected to gain access to an AVNRT circuit unless there's the rare circumstance of a bystander. Again, pretty unlikely. So if it's an accessory pathway, is it right or left-sided? Well, with a barely fused PVC, one would not expect a right-sided accessory pathway to block with a left-sided PVC. Same would be true the other way around if this were a right-sided PVC, one wouldn't expect a left-sided accessory pathway to block because it's too far away. So a barely fused PVC from the left ventricle would be most likely to block a left-sided accessory pathway. So I think you can scour telemetry. And this is something I've really learned as I've gotten older in this field, is that there's a lot of information in telemetry strips. It takes time to go back over them, to scour through, find all the strips, but these full disclosure telemetry systems allow you to do that. You can go back and find key findings and kind of, first of all, it's fun. It's another way to look at things without having intracardiac tracings, but you can use a lot of the same exact principles that we learned from doing EP studies and apply them to surface CCGs. All right, case two. Following pulmonary vein isolation for persistent AFib, the integrity of the roof and anterior mitral lines, represented by dark circles in figure 6-1, is being tested by recording from the distal ablation catheter electrodes in the middle of the posterior left atrial roof, arrow in figure 6-1, and pacing from a multi-electrode catheter in the left atrial appendage, star in figure 6-1. Which is the best answer for the observation in figure 6-2? Roof and anterior mitral lines show conduction block. Only the roof line is blocked. Only the anterior line is blocked. Neither line is blocked. Differential pacing would be required to be sure. So figure 6-1, we have a representation of the line of ablation we've created. We have a recording catheter here and a pacing catheter here. And we have this particular pattern. So this catheter is in the appendage pacing. We have the coronary sinus. And then the ablation catheter is recording on the other side of that line, right here. So how can we interpret this? Well, the first thing you notice is that the splits here are pretty narrow. So that's really suggestive that when you're pacing from here, these splits should be pretty wide. First of all, conduction to here would be relatively quick. And then you'd have to go all the way around the atrium to come back. So these splits should be wide. Second thing you notice is that first component of the A across is early. So one wouldn't expect that if this line were blocked. So if you had a line of block like this first, you wouldn't be able to get to this line except to go all the way around. So that's timing to the first component should be late. And it's not. And then the two splits are early, suggesting that there's also conduction through. So there's conduction both through this line to produce the first early A, this one. And then there's conduction not only through that line to produce the first early A, but then through this line to produce the next early A. The splits are too narrow. So that split is also too early. It's sneaking through that roof line. So we basically have work to do because neither line is blocked. Now you could do differential pacing, but I don't think it's necessary to know that these two lines are not blocked based on the observations we just made. Important here is that a split time of approximately 80 milliseconds was associated with roof block, at least in one study, and these are only 50 milliseconds apart in timing. What we see when we ablate at the roof is that the splits now indicate roof block because the first timing doesn't change. So we're still coming through that anterior line that went from the left superior to the mitral annulus but we're no longer going through the roof line. We get a sudden jump out in atrial activation that would indicate roof block much longer, 150 millisecond splits rather than 50 milliseconds. But we still have to, if we want to block that anterior line, we still have more work to do there. So that's another piece of work that still needs to be done in that case if you want to achieve it. So here's case three. This tracing is obtained during atrial pacing 20 milliseconds faster than the tachycardia cycle lane. Before atrial pacing, there was one-to-one concentric atrial activation associated with each QRS complex. The observation is reproducible. Which of the following is the most likely diagnosis? Bundle branch re-entry, antedromic AV re-entry, SVT with bundle branch aberration, left bundle branch aberration, ventricular tachycardia from the right ventricle, ventricular tachycardia from the left ventricle. Here's your tracing. Again, we're pacing the high RA at a cycle length of 300 milliseconds. The tachycardia is at 320. Here's the measurements from V to V in the RV apex, 320, 320, 320, 320. And then something happens. And what is that? Tachycardia terminates. This is consistent with antedromic AV re-entry. And why is that? Well, first of all, when we pace the atrium, we terminate tachycardia without affecting it first in the ventricle. So how do you do that? So if you had VT, bundle branch re-entry, you would expect that to affect VT, you first have to go through the AV node and pull in the V so it terminates the VT. But that doesn't happen. It's just sudden termination of this wide complex tachycardia from the A. Well, how would that happen? Well, if you're coming over an accessory pathway antegrade, you could block in that pathway by having an atrial wavefront reach the pathway earlier than the tachycardia would. And when it finds it refractory, it blocks in that pathway, which is what happens on this beat. And then this beat conducts through the AV node to the next QRS. So this one is not pre-excited. This is. This was a pretty unusual case. In fact, at other times, we were able to show that it was decremental. And I'll show you a tracing of that. This is the explanation and I'll pause here for a second so you can read it. This was interesting because unlike most decremental pathways, they're usually atrial fascicular, they insert at the RV apex. This one was decremental, but inserted at the base. It had a left bundle morphology indicating it was on the right side and sort of a superior axis. So the decremental conduction prior to termination is shown here, where we have atrial pacing. Last time, the last tracing we saw, we got block in the pathway. Here, we just get delay in the pathway before it blocks on the next beat. So behavior here shows that it's a decremental pathway, antegrade only in this particular case. When we tested to see what the retrograde pathway was, parahysian pacing demonstrated it was the AV node and not another pathway or the same pathway going retrograde. Here's the atrial activation sequence. And when we lose capture of the his, the VA time jumps out, or the stim A time jumps out. Case four, this is a 72-year-old man with extensive left atrial scarring and recurrent one-to-one atrial flutter following multiple ablations. Because of that, he underwent successful AV node ablation and placement of a pacemaker. The 12-lead ECG immediately after the procedure is shown in figure one. Which of the following is most likely? The ventricular lead captures the his bundle directly. The ventricular lead captures the his bundle and local RV myocardium. The ventricular lead captures RV myocardium alone. The ventricular lead captures near the left posterior fascicle. The AV junction ablation has failed and there is native conduction. Here's your tracing. I'll pause for a second. And I think the best answer is that it captures near the left posterior fascicle. In fact, it probably captures the left posterior fascicle directly, honestly. And what are the features that tell you it's not capturing the his bundle, that it's capturing the his Purkinje system in some location, but not the his bundle itself? First of all, the PACE complex is narrow, measures about 100 milliseconds. It has a PACE LV activation time of less than 80 milliseconds to V5. So if we go back and look at that, you can see that the stem here to the activation in lead V5 is quite short, well less than 80 milliseconds, probably on the order of, you know, 50 milliseconds. The total duration is 100 if you measure it from the stem to the F. But there's also a little iso, maybe slight isoelectric interval in most leads. Maybe there's a little Q wave there, probably not much of an isoelectric interval here. So it would indicate that where the exit from this stimulus is from or near the left posterior fascicle, it sort of has a superior axis. The other key to telling you this isn't his bundle capture is this QR. So this pattern occurs when you get through the septum to the left side of his Purkinje system. You get this QR pattern in V1 that you don't see with his bundle capture directly. His bundle capture directly should give you exactly the same QRS as conducted. It also doesn't look like this is a conducted QRS. This QR is an unusual pattern, wouldn't be expected to be seen with native conduction. So it's unlikely the AV node ablation has failed. It's unlikely that this then is pseudofusion. What is pseudofusion? Pseudofusion occurs when there's native conduction and the pacing spike isn't producing anything because it's coming at a time when the ventricle's already been depolarized at that site. So it almost always, the way that happens is the pacing spikes in the QRS slightly. And it's at a spot where since the ventricle's already been depolarized at that location, it's refractory. So the pacing spike isn't capturing anything. So it's not fused at all. It's pseudofused. There's no capture from the pacing spike. You can only tell that if you come off the pacing and see that the QRS is, looks exactly the same as the one that looked like it might have been paced and fused. So I think the best answer is, again, we're capturing near or on the left posterior fascicle in this case. Again, I'll let you look at this explanation. And this is a good reference for you to look at concerning left bundle pacing. Thank you. Welcome to Workshop 5. I'm Bill Stevenson from Vanderbilt University Medical Center. These are my disclosures. Case 1, a 72-year-old male with history of old inferior wall myocardial infarction presents to the emergency room with palpitations and dyspnea. The EKG in tracing 1 is recorded. Following cardioversion, EKG in tracing 2 is recorded. Which one of the following is the most likely tachycardia mechanism? A, reentry in the prior infarct scar, B, bundle branch reentry, C, AV reentry, or D, AV nodal reentry? Here is the first 12-lead electrocardiogram showing the tachycardia. Here is the second 12-lead electrocardiogram following conversion to sinus rhythm. You can pause the video and analyze these and select your answer. So this is an example of bundle branch reentry tachycardia. The 12-lead EKG of the tachycardia shows a wide QRS regular tachycardia with a left bundle branch block configuration with a morphology that's actually typical of left bundle branch block. Brisk downstroke in the anterior precordial leads and a normal frontal plane axis even. However, there is AV dissociation as indicated by the P waves that you can see periodically in the tracing, which are dissociated from the QRS complexes. So that makes a supraventricular tachycardia with aberrancy very unlikely. Occasionally, one can see this with junctional automatic tachycardia, which is more commonly encountered in children, but would be rare in an adult. And when converted to sinus rhythm, he had the same QRS morphology as was observed during tachycardia, consistent with the fact that he's got conduction antigrade down the right bundle, but it's quite slow conduction in the left bundle, producing a pattern of left bundle branch block and sinus rhythm. However, conduction was present in the left bundle briskly in the retrograde direction to allow for bundle branch reentry. And many patients with bundle branch reentry have a left bundle branch block or interventricular conduction delay in sinus rhythm and then left bundle branch block configuration of the VT, as was the case here. Case two, pacing is performed at the right ventricular apex during tachycardia shown in the tracing. Which one of the following is the most likely tachycardia diagnosis? A, bundle branch reentry, B, AV nodal reentry with aberrancy, C, VT from the right ventricular apical septum, or D, AV reentry? Here is the tracing. And you can pause that for analysis and then select your answer. The correct answer is AV reentry. So we have a one-to-one tachycardia with a wide QRS. In the HISS leads, we do not see a clear HISS deflection in front of the QRS complexes. So this could be ventricular tachycardia with one-to-one VA conduction. Or it could be a pre-excited type of tachycardia. During ventricular pacing, you can see that we accelerate the atrial electrograms up to the paced cycle length. And that advances the atrial electrograms and advances the tachycardia. There is a post-pacing interval of 500 milliseconds, which is only 80 milliseconds longer than the tachycardia cycle length. So that's too short for AV nodal reentry. And it's too long for a tachycardia that's originating near the pacing site at the right ventricular apex. It's also too long for bundle branch reentry, because pacing at the right ventricular apex is close to the insertion of the right bundle. And the post-pacing interval from there during bundle branch reentry is usually less than 30 to occasionally 50 milliseconds longer than the tachycardia cycle length. So by process of elimination, then, this is most likely an AV reentry tachycardia. This slide shows you what's going on. The schematic up at the upper right, pacing from the right ventricular apex, produces a post-pacing interval that exceeds the tachycardia cycle length, in this case, by only 80 milliseconds. And the way to sort this out, of course, is to pace in the atrium. And when you do that with a pre-excited tachycardia, you find that the atria can drive the ventricles with no change in the QRS morphology during pacing compared to tachycardia. And if you're pacing close to the reentry circuit site, close to the insertion of the pathway, you'll have a post-pacing interval that will be close to the tachycardia cycle length. So in this case, pacing in the right atrium, the post-pacing interval exceeds the tachycardia cycle length by only 40 milliseconds. This table summarizes for you differences between antedromic tachycardia and ventricular tachycardia. So both are wide complex tachycardias that can have one-to-one AV relationship. In antedromic tachycardia, if you can see activation of the His bundle, it will be consistent with retrograde activation, unless multiple pathways are present providing more than one route for retrograde conduction. And in ventricular tachycardia, this bundle will also be activated retrograde if you can see it. Ventricular pacing will entrain both of these tachycardias if they're reentrant. And both of them produce an AV type of response. So ventricular pacing for wide complex tachycardia, that's VT versus an antedromic tachycardia, is not helpful. The post-pacing interval can be relatively short for both of them. If you are near the reentry circuit in the ventricle or near the reentrant path for the AV reentrant tachycardia, the thing that's really helpful is atrial pacing, which will advance the QRS without changing the QRS morphology. In contrast, when you apace during ventricular tachycardia, that will dissociate the atrium from the ventricle, in most cases, or cause fusion. And rarely, if you have a Purkinje-related ventricular tachycardia, you may be able to entrain that from the atrium if AV nodal conduction is very good. And then the post-pacing interval tachycardia cycle length will be close to the circuit, approximating the tachycardia cycle length in antedromic tachycardia if your atrial pacing site is near the accessory pathway. But in ventricular tachycardia, no matter where you pace in the atrium, the post-pacing interval is going to be very long if you do advance the ventricles to the paced cycle length. Case three, activation maps are obtained from three different VTs in three different patients, shown in the three panels of this figure. Which one of the VTs is most likely due to automaticity? So here are the tracings for you to pause the video, analyze. These are all activation sequences, activation maps in electroanatomic mapping systems. You can see that the tachycardia cycle lengths are also provided for you. And you can pause and select your answer. So the correct answer is panel A is most likely to be a focal origin tachycardia. So you can see here that in panel A, we have an activation map. Activation proceeds from earliest being red, and then through the colors of the rainbow, yellow, green, blue, purple, to progressively later. And we have a small area of red, which is the area of the tachycardia. And we have a small area of early activation. And then activation spreads out in all directions away from that site. The tachycardia cycle length here is 280 milliseconds. And you can see that the total duration of activation that was identified with this activation map is only 185 milliseconds. So doesn't it outline the tachycardia cycle length? The middle panel shows an activation map which is consistent with a focal breakout area on the endocardium, the lower panel. We have an area of early activation, and then activation spreads out in all directions from that site. But in the epicardium, we have activation that spans the cardiac cycle going from minus 46 to 243 milliseconds, so approximately 290 milliseconds with a tachycardia cycle length of 310. And we have an area of earliest activation butting up against latest activation. So this is consistent with reentry. This is then consistent with epicardial reentry with a focal endocardial breakthrough site. And then in the right panel is another example of a reentrant tachycardia. This was also an epicardial tachycardia where we have a circuit that's revolving around in this direction with an early meets late site and almost a complete tachycardia cycle length accounted for in the activation sequence map. Case four, a 58-year-old male with non-ischemic dilated cardiomyopathy is referred for catheter ablation of the arrhythmia shown in the tracing. Which one of the following sites or regions is likely to require ablation to abolish this tachycardia? A, the right bundle branch. B, lateral left ventricular epicardium. C, the inferior left ventricle epicardium. Or D, the anterolateral LV papillary muscle. Here is the LV EKG. You can analyze that, pause, and select your answer. So this is a VT that comes from the lateral left ventricle, likely from the epicardium. So in assessing the origin of a ventricular arrhythmia, I have a relatively simple system. First look at V1. If V1 is left bundle branch block-like in configuration, that tells you that you've got early activation of the anterior portion of the ventricle, either the right ventricle or the interventricular septum. And if you have a right bundle branch block configuration in V1, that tells you you have a left ventricular origin. Then you look at the frontal plane axis, and if you activate the heart in its cranial aspect in the anterior aspect, you get a vector which is directed inferiorly. So you expect to have dominant R waves in the inferior leads, 2, 3, and AVF. If you initially activate the diaphragmatic surface of the heart, you get dominant S waves in leads 2, 3, and AVF due to the vector moving from low to high. And you can refine this by looking at other aspects of the QRS axis. If you activate the lateral wall, you expect to produce a prominent vector going rightwards, so away from the left shoulder, giving you a dominant S wave in 1 and AVL. And then to get your orientation in the base-to-apex direction, you look at leads V3 and V4, which are over the left ventricular apex. And if you have early activation, initial activation at the apex beneath those leads, you expect a vector which is moving away from V3 and V4, so you get dominant S waves in those leads. In contrast, when you activate the basal portion of the ventricle, you have a wavefront which is moving towards V3 and V4, so you expect dominant R waves in those leads. And then why do we say that this is epicardial? Well, this patient has a non-ischemic cardiomyopathy, so that increases the chance that you may have to go to the epicardium. But there are some EKG markers that can be suggestive as well in non-ischemic cardiomyopathies. Because the epicardium is further from the Purkinje system, the QRS complex will tend to be wider. And if you initially activate the epicardium and you are recording from leads that reflect the activation of that region, the wavefront will be going towards the endocardium, from epicardium to endocardium, so that the initial activation will be going away from those leads. So in the lateral wall of the left ventricle, if you have an epicardial focus out there, you expect to have a QS-like configuration in lead 1 and AVL, as the wavefront is going away from the epicardium, the lateral epicardium. In contrast, if you have a focus that's endocardial, you have initial activation spreading from endocardium to epicardium, and you expect to see at least a small initial R-wave in those leads. Now, the slow activation through the epicardium can also produce a pseudo-delta wave sort of appearance with a slurred QRS upstroke in some of the leads. Very important to recognize that these are only rough guidelines and that we've all seen many exceptions to the QRS morphology suggesting an epicardial versus an endocardial origin. This is not at all reliable in coronary artery disease, where you often have large, relatively confluent scars. But in non-ischemic cardiomyopathy, the finding of a QS complex in leads 1 and AVL, when you've got lateral basal scar and a VT that's a right bundle, right axis configuration, is suggestive of a possible epicardial exit. This is relevant because epicardial mapping and ablation may be required for that VT. Case 5. A 72-year-old male with coronary artery disease is referred for catheter ablation of the arrhythmia shown in the tracing. Which one of the following sites or regions is likely to require ablation to abolish this arrhythmia? A, the basal LV septum, B, the apical LV septum, C, the infralateral LV epicardium, D, the infralateral LV endocardium, E, the anterolateral LV endocardium. Here is the 12-lead EKG. And you can pause and consider your options and select. So the answer is infralateral LV endocardium. Now this is a patient with coronary artery disease. So the QRS morphology criteria for endocardial versus epicardial, as we just discussed, is not reliable. This tachycardia is right bundle branch block in configuration in V1, consistent with its left ventricular origin, has a superiorly directed frontal plane axis, consistent with origin from the inferior wall. And that's where the infarct is. So even though it's relatively wide and slurred, this will likely be approachable from the LV endocardium in the inferior wall. Case 6, a 35-year-old female with exercise-induced syncope undergoes electrophysiologic study. The tracing shown is recorded during isoproteranol infusion. Which one of the following is the most likely diagnosis? A, arrhythmogenic RV cardiomyopathy, B, cardiac sarcoidosis, C, lamin A-C cardiomyopathy, or D, idiopathic VT. Here is the 12-lead EKG from the EP lab with the right atrial and right ventricular electrograms shown at the bottom, recorded during isoproteranol infusion. And you can pause and select your answer. So this is arrhythmogenic right ventricular cardiomyopathy. You can see that the patient is having polymorphic ventricular tachycardia, which has occurred spontaneously during the isoproteranol infusion. And this is seen commonly in arrhythmogenic right ventricular cardiomyopathy that has a genetic cause. It is not a typical feature of the other diseases mentioned. Idiopathic VT is usually monomorphic. And this has been proposed as a possible diagnostic criteria for ARVC, but has not been fully adopted yet. And we can apply our EKG analysis to where is that VT coming from. And although polymorphic, the QRS complexes were largely left bundle branch block in configuration. So again, consistent with the right ventricle or the interventricular septum. And VTs that originate from that area, Purkinje-related tachycardias, LV septal tachycardias, but then everything else is right ventricular origin, idiopathic VTs, or scar-related. And things that produce scar in the right ventricle are genetic ARVC, sarcoidosis, and then much less frequently, right ventricular infarctions or surgically induced right ventricular scars as may be seen after repair of Tetralogy of Fallot. The left bundle branch block configuration of VT, as we mentioned, suggests a right ventricular origin. And there are some features that can help you distinguish between an idiopathic right ventricular VT and a scar-related right ventricular VT. So first, any sinus rhythm EKG abnormality suggests possible underlying structural disease and points you towards a disease process that would be consistent with a scar-related VT. Most idiopathic right ventricular VTs originate from the right ventricular outflow tract. So they have a relatively QRS configuration that reflects that with a transition that's often before V4. So you have a dominant R wave in V4, V5. If you have a later transition, that suggests an origin down lower in the right ventricle that would be more commonly seen with scar-related VTs. In idiopathic VT, the QRS complexes are often nice and brisk in their downstroke in the precordial leads, whereas it may be slurred with scar-related VT. And QRS configurations having more notches would be more consistent with a scar-related VT. Idiopathic VT is almost always one focus. It's unusual to see multiple morphologies of an idiopathic VT, whereas it's common to see multiple morphologies of VT in structural heart disease. And isoproterenol is often required to initiate idiopathic VTs, but as we've already discussed, this can also be the case for arrhythmogenic right ventricular cardiomyopathy, which is a scar-related VT in most cases. Case 7, a 48-year-old male with recurrent episodes of wide complex tachycardias for several years is referred for catheter ablation. He has no family history of sudden death or heart failure. Echocardiogram shows normal LV ejection fraction of 50% and mild right ventricular enlargement. The EKGs of tachycardia are shown in the first figure, and the second figure shows the 12-lead EKG after cardioversion. Which one of the following is the most likely diagnosis? A, arrhythmogenic right ventricular cardiomyopathy, B, cardiac sarcoidosis, C, lamin A-C cardiomyopathy, D, idiopathic VT. Here is the 12-lead EKG of the tachycardia, and here is the 12-lead EKG following conversion. You can pause the video, toggle back and forth if you need to, and make your selection. So this patient has cardiac sarcoidosis. Sarcoidosis is a relatively rare disease that is due to the formation of non-caseating granulomas that can affect any organ of the body, but it can affect the heart, and it can affect preferentially the right ventricle. When it affects only the heart, it can be a very difficult diagnosis to make. And it is often progressive and is associated with a significant mortality risk. It can affect any part of the heart, so it can cause conduction abnormalities, in this case right bundle branch block. It can affect AV conduction and cause heart block. Ventricular arrhythmias is a major concern. These are scar-related reentry due to the areas of scar in the ventricle that can affect either the left or the right ventricle. Atrial arrhythmias are encountered as well. Atrial tachycardia is atrial fibrillation, atypical atrial flutters. And a very useful diagnostic evaluation is sarcoid PET scan, which is to assess the uptake of glucose in the heart after the patient has had a zero-carbohydrate diet for one to two days. This suppresses glucose uptake in the heart, and any glucose uptake that is present is then likely from the presence of inflammatory cells, hence this is an indication of inflammation. Now, sarcoidosis can mimic arrhythmogenic right ventricular cardiomyopathy. It can meet all of the task force criteria, and there are many cases in the literature and all transplant programs, I would venture to say, have seen cases of a patient who is referred as being sarcoid but turned out to have arrhythmogenic right ventricular cardiomyopathy and vice versa. Sarcoid is favored by older age presentation and evidence of septal involvement. The septum is often spared in arrhythmogenic right ventricular cardiomyopathy, so AV block, evidence of scar in the septum on MR imaging or in the electrophysiology laboratory. A family history of disease is also favoring arrhythmogenic right ventricular cardiomyopathy. So our patient, let's just look back here again, has a left bundle branch block inferior axis VT that looks like it would be coming from the right ventricular outflow tract. So this could be idiopathic, although the QRS is relatively wide, and when he's converted, he has right bundle branch block with first degree AV block and a very long PR interval. So clearly some underlying structural heart disease associated with an AV conduction abnormality. So of the choices that you have, the most likely thing is cardiac sarcoidosis. Arrhythmic cardiomyopathy typically does not prominently involve the right ventricular outflow region. It does involve the septum very prominently and can produce heart block. And there's evidence of clear structural abnormalities in the sinus rhythm EKG, so this is unlikely to be idiopathic VT. Case 8. A 67-year-old male undergoes mapping for intended ablation of post-infarct VT. During VT, the blood pressure is 83 over 48 millimeters of mercury. Pacing is performed as shown in figure 8-1. Which one of the following is the most reasonable next step? A, ablate at this site, B, terminate VT and proceed with substrate-guided ablation, C, pacing at this site with greater stimulus strength, or D, repeat pacing at this site at a faster rate. Here is the tracing and you can pause and analyze and make your selection. So the answer is to ablate at this site. You don't have a lot of time because he's hypotensive. But pacing here, even though you cannot see much of an electrogram, there's this tiny little potential here, pacing actually captures and advances the QRS complexes and the right ventricular electrograms up to the pacing rate. We have entrainment with concealed fusion, a stimulus to QRS of 180 milliseconds, and if we march back 180 milliseconds, we can see that there is this little signal here. It's kind of coming and going a little bit, varying in amplitude about 160 milliseconds before the QRS. So this was a site in the reentry circuit isthmus and it just makes the point that you can have very low amplitude signals in some of these scar-related reentry circuit isthmuses and your mapping system may gloss over these. If you pace, you may in fact discover that this is a site that requires ablation to interrupt the tachycardia. And here again, just with the intervals indicated for you to convince you that we really did accelerate those QRS complexes up to the pace cycle length. Case 9. Epicardial mapping is performed in a 50-year-old male with non-ischemic dilated cardiomyopathy and recurrent VT. The activation map during VT is shown in figure 1. During VT, pacing is performed from the ablation catheter at one of the sites indicated by the letters, and that's shown in figure 2. Which one of the sites labeled in figure 1 is most likely the pacing site shown in figure 2? So here is our diagram. This is the epicardial activation during ventricular tachycardia. You can see how the mapping window for the electroanatomic mapping system is configured here on the right-hand panel and the sites labeled A through D. And then the second tracing shows a pacing at the site during tachycardia. You can pause the video and analyze these and select your answer. So the pacing features suggest that we're at site D, which is near the outer loop just beyond the exit of this reentry circuit. So here is that tracing. You can see that pacing accelerates the QRS complexes up to the pace cycle length of 520 milliseconds. The post-pacing interval is 560 milliseconds, only 20 milliseconds longer than the tachycardia cycle length. So we're pretty close. We're in the reentry circuit. Now do we have a change in the QRS? And we do. The QRS morphology is a little bit different, subtly so, but definitely different than during VT. There is a little bit of delay between the stimulus and the QRS. So this is consistent with pacing in an outer loop. The timing of activation at this site is at the onset of the QRS. So this outer loop region just beyond the exit is likely where we're located. And this would be a case where we would then try and find a site probably moving back in more towards the center of the scar where we would hope we would be able to find the isthmus region for this VT if we were able to map during the ventricular tachycardia. Thank you.
Video Summary
In the first case, the video presenter discusses a patient with wide complex tachycardia and presents the ECG tracings and intracardiac recordings during burst pacing from the right ventricular apex. The correct diagnosis is bundle branch reentrant ventricular tachycardia, determined by analyzing the surface ECG and intracardiac recordings that show evidence of fusion, activation sequence, and post-pacing interval. In the second case, the presenter discusses a patient with recurrent atrial fibrillation in response to isoproterenol. The EKG shows a triggered atrial fibrillation originating from the superior posterior wall of the left atrium. The correct site of the non-pulmonary vein trigger is the superior posterior left atrium between the isolated pulmonary veins. In the third case, the presenter discusses a patient with a wide complex tachycardia during atrial pacing 20 milliseconds faster than the tachycardia cycle length. The correct diagnosis is bundle branch reentry tachycardia, determined by the fusion seen during pacing and the post-pacing interval. In the fourth case, the presenter discusses a patient with recurrent VF episodes following acute myocardial infarction. The correct diagnosis is bundle branch reentry tachycardia, determined by the QRS morphology and the evidence of concealed fusion during entrainment. In the fifth case, the presenter discusses a patient with a history of palpitations and dyspnea. The correct diagnosis is AV reentry tachycardia, determined by the evidence of concealed entrainment during pacing and the activation sequence during tachycardia. In the sixth case, the presenter discusses a patient with ventricular tachycardia following pulmonary vein isolation. The correct diagnosis is idiopathic ventricular tachycardia, determined by the QRS morphology and the evidence of termination with pacing. In the seventh case, the presenter discusses a patient with recurrent wide complex tachycardias. The correct diagnosis is arrhythmogenic right ventricular cardiomyopathy, determined by the QRS morphology, the evidence of AV dissociation, and structural abnormalities seen in sinus rhythm. In the eighth case, the presenter discusses a patient with post-infarction ventricular tachycardia. The correct next step is to terminate the tachycardia and proceed with substrate-guided ablation, as pacing at this site has already been shown to capture and therefore ablation at this site is likely to be successful. In the ninth case, the presenter discusses a patient with non-ischemic dilated cardiomyopathy and recurrent ventricular tachycardia. The correct diagnosis is cardiac sarcoidosis, determined by the QRS morphology and evidence of scar in the lateral wall of the left ventricle.
Keywords
wide complex tachycardia
bundle branch reentrant ventricular tachycardia
ECG tracings
intracardiac recordings
fusion
activation sequence
post-pacing interval
recurrent atrial fibrillation
isoproterenol
triggered atrial fibrillation
non-pulmonary vein trigger
atrial pacing
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