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Session II: Invasive Diagnosis and Treatment-6154
Principles of Entrainment- Ventricular Tachycardia
Principles of Entrainment- Ventricular Tachycardia
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Video Transcription
This session is on principles of entrainment for ventricular tachycardia mapping. I'm Bill Stevenson from Vanderbilt University Medical Center. These are my disclosures. So with the activation maps that we can now create with modern electroanatomic mapping, we're getting to see more and more examples of reentry circuits in scar-related reentry. And very often, they appear to take the form of a double loop sort of a circuit, a figure eight sort of a circuit where a wavefront emerges from an isthmus, propagates in counterclockwise and clockwise directions around the isthmus, and then returns to the isthmus through what we refer to as an entrance. And these circuits form in areas of scar. So on the right-hand side here, you see a voltage map that shows an area of low voltage consistent with a scar that contained this reentry circuit that's illustrated in the activation sequence map on the left. A schematic summarizing another double loop reentry circuit is shown at the far left. And note that here, I've tried to indicate that the activation sequence map is color-coded such that the exit is activated first, is early, shown in red, and then activation spreads through the colors of the rainbow, yellow to green to blue to purple, and that's what you would expect it to look like. Now if you compare that with the activation map that we see in the center, you can see here the exit is not the earliest part, right? It's blue, but the sequence is consistent. And this is just to make the point that the colors that are displayed are determined by the timing that is set by selecting the reference point and the mapping window. So that looking at these activation sequences in a propagation sort of map can be helpful rather than just looking at the times. And so if we play the propagation map of this, you can appreciate very easily that this is a figure of eight type of reentry circuit, even though we've got this funny early activation in red located not out at the exit region. So activation maps and their interpretation can be complex. But if you can find a reentry circuit isthmus, the likelihood that ablation of that isthmus will abolish VT is very high. And we've shown that with entrainment mapping over the years. And now that activation mapping is capable of creating these nice maps, Dr. De La Bella's group has also made that point that if they can define the complete diastolic pathway of arrhythmia, the likelihood of abolition of VT and the risk of recurrence is much lower than if you can't identify the diastolic isthmus of the tachycardia. Now entrainment allows you to recognize parts of the reentry circuit. You don't need to create the entire activation map. And that's important because very often we only get to see a portion of the reentry circuit. So here's our figure eight reentry circuit in this diagram on the left. But you can see that the circuit's intramural. And there's a breakout on one surface, which gives you an activation sequence that looks relatively focal, even though you've got a big macro reentry circuit. In the middle panel here, we've got portions of the reentry circuit on the endocardial surface. But the activation map would look like we've got two areas of early breakout. And those occur actually when a loop portion of the circuit reaches this endocardial surface. And the entrance, you wouldn't appreciate easily from analysis of the activation map at all. And then you can also have a situation where you have a reentry circuit which is remote to the endocardium. And it produces a focal breakout area. Activation mapping would suggest this is a focal arrhythmia, but you're miles away from the reentry circuit site. And so combining activation mapping with entrainment kind of helps you recognize these situations. So here's another example of an activation map. And in this one, you can see we've got early activation here, and then a wavefront that spreads out counterclockwise and clockwise around this region of breakthrough, suggesting that there should be an isthmus in here. But we don't have an activation sequence that makes sense for an isthmus. You can see we've got a breakout and a wavefront spiraling around, and then late activation over here, and then an area here where we don't have diastolic electrical activity. And this kind of thing is very common in these scar-related arrhythmias because of their three-dimensional nature. And Rod Tung has published a series of papers in which he performed endocardial and epicardial mapping of VTs. And if you look at how often can you define an entire reentry circuit, even with aggressive attempts to map during VT, you find that it's the minority of cases in which the entire reentry circuit can be constructed based on the activation map from endocardial and epicardial mapping. So this is where entrainment is useful. And some years ago when we started evaluating this, we worked from this kind of an anatomic model where we constructed a type of a figure-eight circuit, but where the loops were asymmetrical. And you could have bystander areas that were connected to the loops. You can have a bystander loop where one loop is faster than another loop. And then defined the entrainment responses that allowed you to recognize these different parts of the reentry circuit. So let's talk then about entrainment. So entrainment is the continuous resetting of a reentry circuit. And it was initially defined by Al Waldo, who was studying postoperative atrial flutter using temporary atrial pacing leads and worked all this out in a real tour de force of electrophysiology. So entrainment is the continuous resetting of the reentry circuit. And this schematic shows you what happens. You're pacing at a site which is remote from reentry. The stimulated wavefront propagates to the reentry circuit. And it splits into an orthodromic component, which propagates through the circuit in the same direction as the tachycardia wavefronts. And an antidromic component, which propagates in the reverse direction in the circuit. Now after a few beats, the site of collision of the orthodromic and antidromic wavefront stabilizes. So you have the same proportion of the ventricle activated antidromically and orthodromically on each beat. And that produces QRS fusion. So the QRS morphology will be between that which you expect from the VT and from activation only from the pacing site. And then when you stop pacing, the last stimulated orthodromic wavefront propagates through the circuit and continues the tachycardia. So what you expect to see is shown here. We have ventricular tachycardia at a cycle length of 335 milliseconds. The last three stimuli of a pacing train capture. The QRS complexes are different during pacing and during tachycardia. But they have a stable consistent morphology, which is due to stable fusion. And if you show that you have constant fusion during the tachycardia, that is sufficient to infer that you have entrainment. That's a criteria. Now there are some additional criteria that Dr. Waldo developed, including showing progressive fusion, which we'll talk about. And there's also a characteristic mode of termination of tachycardia that shows that when you get conduction block in the circuit and then activate that region from a different direction that that terminates the tachycardia. We see that from time to time. But we don't generally routinely use it for assessing the presence of entrainment. Because we're usually trying not to terminate the arrhythmia with pacing when we're using entrainment for mapping. Now this is that tracing that I just showed you, where we have pacing that changes the QRS morphology. And following termination of pacing, the tachycardia continues with the previous morphology. This is consistent with entrainment. But if all you have is this tracing, you don't know that you're simply overdrive suppressing an automatic focus. In other words, maybe during pacing, this is what the QRS complex would look like, even if you weren't in tachycardia. And then you stop pacing and the focus just continues firing. In other words, you don't know that this QRS is fused rather than totally paced. So to assess that, sometimes what's required is to either know the QRS morphology during pacing and sinus rhythm, or to change the degree of fusion during pacing. And that is progressive fusion. So in the top diagram, this is the tracing you've already seen that shows pacing at a cycle length of 310 milliseconds during tachycardia. And in the bottom tracing, we're pacing at a cycle length of 280 milliseconds, just slightly faster. And pacing at the faster rate, although it's at the same site, the QRS morphology is very different. The QRSs in the inferior leads now are dominant R waves rather than QS complexes. And that's because this pacing site is actually up in the right ventricular outflow tract. So pacing at the faster rate, the stimulated antedromic wavefront propagates a greater distance before it collides with the orthodromic wavefront. It activates more of the ventricle antedromically. And therefore, during pacing, the QRS morphology more closely resembles that which you expect to see during pacing in the absence of tachycardia. So this is progressive fusion. Pacing at two different rates shows you different degrees of fusion. But the QRS morphology is stable. Fusion at that rate after the first few beats of pacing. Now you can also see evidence of fusion in examination of the electrograms. So here we have ventricular tachycardia, the last three stimuli of a pacing train. And all of the QRS complexes and electrograms are accelerated to the pacing rate. If we analyze the electrogram morphology here at the right ventricular septum, you see that during pacing, the electrogram morphology is substantially different than that during tachycardia. That is evidence that that site is activated by a wavefront which is coming at it antedromically from a direction different than how it's activated during tachycardia. In contrast, at the right ventricular apex, the electrograms are the same morphology during pacing as during the tachycardia. Now also interestingly, in this example at the right ventricular apex, the electrogram which is accelerated to the paced cycle length falls quite a long interval after the stimulus. So in this last stimulus that advances the electrograms to the paced cycle length, this is the last electrogram accelerated to the paced cycle length of 380 milliseconds. And that's consistent with conduction time for the wavefront to go from the pacing site to the reentry circuit and through the reentry circuit before it reaches this site. So this site is activated orthodromically and during pacing, this site, the RV septum is activated antedromically. So on this one beat then, we have evidence of simultaneous antedromic activation and orthodromic activation. And that's the definition of fusion. So this is the electrogram evidence of constant fusion. This is particularly useful for mapping atrial arrhythmias, scar-related atrial arrhythmias. Because there, you can't usually get a sense of fusion from just looking at the surface EKG P waves. Now the first question that we then ask when we know we have a reentrant arrhythmia and we've been able to entrain it is whether we are in the reentry circuit. And the post-pacing interval gives us a quick assessment of the proximity of the pacing site to the reentry circuit. So that is illustrated here, following the last stimulus, which advances the tachycardia to the pace cycle length, wavefront propagates over to the reentry circuit, through the circuit, and then back to the pacing site. So that post-pacing interval from the last stimulus to the next activation at the pacing site then is equal to the conduction time from the pacing site to the reentry circuit, around the reentry circuit, which is the tachycardia cycle length, and then back from the reentry circuit to the pacing site. So the degree to which the post-pacing interval exceeds the tachycardia cycle length reflects the conduction time from the pacing site to the circuit and from the circuit back to the pacing site. So in this example, the post-pacing interval is 520 milliseconds to the earliest electrogram that we see here that could be a local potential. And the tachycardia cycle length is 400 milliseconds. So the difference is 120 milliseconds. That suggests that the conduction time to and from the circuit is perhaps 60 milliseconds if the conduction velocity is the same in both directions, which it may not be. So entrainment mapping tells us, are we in the reentry circuit? And then secondly, we can use it to determine if the site is at a narrow isthmus in the reentry circuit where ablation is likely to be effective. And the post-pacing interval is useful, but there are three things that have to be true for the post-pacing interval to be reliable. First, pacing has to reliably capture. Second, pacing cannot alter the reentry circuit path or the conduction times in the circuit. And third, we have to be able to identify a local electrogram at the pacing site to measure the post-pacing interval to that time. So let's consider some examples. So here is ventricular tachycardia, and you see the last five stimuli of a pacing train. And my question is, what is the relation of the pacing site to the VT? Are we A, in the circuit, B, outside the circuit, or C, cannot be determined? You can pause the video to analyze this and select your answer. So here, entrainment was not useful. In fact, we didn't entrain the tachycardia, and we can't determine the relationship of the pacing site to the circuit because we're not reliably capturing. If you look carefully at the electrograms, you can see that there's a variable relationship between the pacing stimulus and the electrogram. And this can be very subtle because we're often pacing just slightly faster than the tachycardia cycle length because we don't want to terminate the tachycardia, and we don't want to alter conduction in the tachycardia circuit. So the first step is always to put your calipers on the electrograms and make sure that they are accelerated to the pace cycle length in a stable way before you start trying to interpret the effects of entrainment. Here's another example. What is the relationship of the pacing site to the VT? Is it in the reentry circuit, outside, or cannot be determined? You can pause the video and analyze. So this is another indeterminate response because here what's happening is after we stop pacing, the tachycardia cycle length is quite variable. So you see that the post-pacing interval is quite long, 460 milliseconds, but the tachycardia cycle length is varying from 300 to 280 to 350 to 380. So this is an unstable circuit where the conduction in the circuit is varying, and therefore we don't know what to compare the post-pacing interval to, and it's likely that the post-pacing interval is falsely long because pacing may have further slowed or altered conduction in the circuit. And this schematic shows you how that can happen. You pace at a rate faster than the tachycardia. You may induce areas of functional block in the circuit that prolong the reentry path and prolong the post-pacing interval. Or you may just simply slow conduction in the circuit if conduction is behaving decrementally in the reentry circuit. And this happens not infrequently, even in common atrial flutter. Here's another example, ventricular tachycardia, a cycle length of 550 milliseconds, the last three stimuli of a pacing train, and the question is, what is the relation of the pacing site to the VT? Are we in the reentry circuit, outside the reentry circuit, or cannot be determined? You can pause the video for analysis and then answer. So this is outside the reentry circuit. Now the problem here is selecting the appropriate electrogram to measure the post-pacing interval to. So first, the pacing has accelerated all of the QRS complexes and the electrograms to the pace cycle length, and the VT cycle length is stable, so we can analyze this. But then we have a couple of different electrograms at the pacing site. And this large one occurs at 535 milliseconds, close to the tachycardia cycle length. But this one is due to a far field signal. You see that this signal is present and visible during pacing. So there's no way that the tissue that gave rise to that signal was directly captured by our pacing stimulus. So we know that we have to exclude this one. The signal that we do not see during pacing coincides in time with this electrogram. And if that's the local potential, then the post-pacing interval is quite long, 745 milliseconds to the onset of that signal. And one of the issues here is that the recording amplifier is saturated during pacing so that we can't see the signals recorded from electrodes 1-2, our distal bipole. When that amplifier recovers, we can compare those signals to what we see on the proximal electrodes 3-4, and you see that there is this signal present that coincides with the sharper signal present on the distal electrode, which coincides with this signal, which we can consider for measuring the post pacing interval. Now we can't prove which one of these is really the local potential, but we can exclude some of these signals as being far-field and not use those for measurement of the post pacing interval. This is very common during mapping of scar-related VTs, and here's another example. Here we have an example of entrainment with concealed fusion, which we'll review in a moment. And where do you measure the post pacing interval here? Well, the large signal here is this one, but you can see that it is visible during pacing and is generated by tissue that's depolarized at some distance from the pacing site. The local signal is somewhere in this low amplitude fractionated signal, and that's the signal that's relevant for entrainment mapping. You want to exclude those far-field potentials. Here's another example, which is really quite dramatic. So here's VT, and you see the last two stimuli of a pacing train. All of the electrograms and QRS complexes are accelerated to the pacing rate, but what is the local potential? Well, it ought to be this large sharp thing, but you see that we're not actually capturing that. It's visible during pacing, and probably what we're capturing is this low amplitude signal indicated by the arrow. And again, we have saturation of the amplifier from the distal electrodes that prevents our ability to see that electrode very well. So when this is the case, how do you determine the post pacing interval? One option is, as we did on the last example, to see what signals are present on the adjacent electrodes, assess whether a signal that is consistent with that signal is also present on the distal electrode, and use that measure to the proximal electrodes as you see here. Another option is to use two cycle lengths and measure the post pacing interval two cycle lengths away. And then another option is to use what's called the stem to QRS N plus one to measure the stimulus to QRS to a QRS complex one interval after the last complex, which is accelerated to the paced cycle length, the N plus one complex. And let me show you how that is done. So here we have an example of a VT. The pacing train accelerates all of the QRS complexes and electrograms to the paced cycle length, and it's difficult to see the electrograms here at the pacing site as the amplifier is slowly recovering from from saturation. So we measure the stimulus to QRS to a nice reference point that's well-defined on the QRS complex, which is not fused. That's our stem to QRS N plus one interval of 640 milliseconds in this case. We then take that, our calipers, and move rightwards to a point where the recording amplifiers are recovered so we can see the signals well. And we identify that same reference point on the QRS complex. And then we measure backwards 640 milliseconds and identify that point, which is identified by that measurement, and assess whether there's a possible local electrogram at that site, as you see here. The difference between this point and the nearest local electrogram equals the post pacing interval tachycardia cycle length difference. It's awkward to explain, but it's very easy to do with electronic calipers in the electrophysiology laboratory. Now another feature of pacing that one can assess to give you an idea of how close you are to the reentry circuit is how quickly the pacing train interacts with the tachycardia reentry circuit. Now when you entrain the tachycardia, you should set your stimulator so that the first beat of the pacing train falls at a consistent time late in diastole. And typically you select the interval to be equal to the pace cycle length and then sense off a ventricular electrogram. And what you hope is that you'll get the first stimulus to fall late in electrical systole. If that's the case, then the number of stimuli that it takes before you begin resetting the tachycardia is related to how close you are to the reentry circuit. And that's illustrated in these diagrams. So if we're pacing remote from the circuit, the first stimulus that falls late in diastole collides with a wavefront from the reentry circuit, doesn't work it, doesn't reach it rather. The next stimulus falls a little bit earlier in the, as with our pacing train, and goes a little further. The third stimulus of the pacing train now goes even further and it may reach the reentry circuit. So the closer you are to the circuit, the fewer number of stimuli are required before you start seeing advancement of the tachycardia QRS complexes. So this is the concept of the number needed to entrain. And it's been shown for atrial arrhythmias. And this is from this nice paper published a few years ago. You can see that the smaller the number needed to advance the tachycardia, the shorter the post pacing interval tachycardia cycle length difference is likely to be. And there's quite a good correlation there. Okay, now the post pacing interval tells us if we're in the reentry circuit or not, but it does not tell us if we're at a narrow part of the reentry circuit where ablation can interrupt reentry. It does not distinguish an isthmus site from an outer loop type of site where ablation is not capable of interrupting reentry. The post pacing interval will approximate the tachycardia cycle length at both of these sites. So how do we distinguish a central isthmus site from a loop kind of site? And for that we look at fusion, which is a reflection of how the stimulated antedromic wavefronts can propagate away from the pacing site. So when we're in an outer loop, the stimulated wavefronts can propagate out away from the reentry circuit, changing the activation of the ventricle remote from the reentry circuit and producing a change in the QRS morphology. In contrast, when you're pacing in an isthmus, the stimulated antedromic wavefronts are constrained by collision with the returning orthodromic wavefronts and by the surrounding areas of conduction block that define the reentry circuit isthmus. The stimulated orthodromic wavefronts can exit from the circuit only from the same exit that's used during the tachycardia. So the QRS complexes are accelerated up to the pacing cycle length and they remain identical to the tachycardia QRS complexes. In other words, the fusion is concealed in or near the reentry circuit where the stimulated antedromic wavefront is colliding with the returning orthodromic wavefronts. And you may be able to detect it only from recording the electrograms in that region where there is some antedromic activation. So here's an example again of VT and the last four stimuli of a pacing train. The pacing accelerates the QRS complexes and electrograms up to the pace cycle length. And the post pacing interval here, I will tell you, is this is the example that we just reviewed a couple of slides ago and it's in the reentry circuit. So the question is, are we in an isthmus or are we in a loop where we're not going to be able to interrupt VT? So you can pause the video and analyze that. Well, here we're in a loop. So the post pacing interval indicates that we're in the reentry circuit. And then the question is, do we have QRS fusion? And you want to look carefully at the QRS complexes and I would argue that the QRS here in lead 1 is different during pacing than during tachycardia. You can see that it's narrower. And there are subtle differences in leads 2 and 3 as well with the loss of this little notch in the inferior aspect of it. If we show you the 12 lead EKG, it's even more evident. So you see that in the mid precordial leads, there's really quite a substantial difference in the QRS morphology during pacing as opposed to during VT. There's also a very short stem to QRS interval here, which is consistent with pacing and tissue where the conduction is relatively brisk. So this is pacing in an outer loop site of the circuit. Now, in contrast, this schematic shows you what you expect pacing at a site which is in a reentry circuit isthmus. During the pacing, the antidromic wavefront collides with the returning orthodromic wavefront in or near the reentry circuit. The stimulated orthodromic wavefronts exit at the same region as the tachycardia wavefront so that the QRS morphology remains the same during pacing as tachycardia. The post pacing interval, which reflects one revolution through the circuit, thereby equaling the tachycardia cycle length. Now, in addition, when you have entrainment with concealed fusion, the stimulus to QRS interval equals the conduction time from the pacing site to the exit of the circuit. That equals the electrogram to QRS onset interval during the tachycardia, reflects the same conduction time. So the stim to QRS equals the electrogram to QRS, and that's another indication that you're in the reentry circuit. So here is an example. We have ventricular tachycardia at a cycle length of 360 milliseconds, the last three stimuli pacing at a cycle length of 330 milliseconds. The QRS complexes and electrograms are accelerated to the pace cycle length. The stimulus to QRS interval is 180 milliseconds. The QRSs are the same during pacing as during tachycardia. In entrainment with concealed fusion. If we take that stim to QRS of 180 milliseconds and go back 180 milliseconds from the onset of the QRS to the recording on our distal ablation electrodes, we see that that lands on this low amplitude signal here. So the stim to QRS, if this is the local potential, matches the electrogram to QRS. And you can see that there's a far field potential, this large signal here, which we know to ignore because we can see that during pacing where it's not perturbed. So this is clearly a far field potential. If we increase the gain of our recording, that's what you see in this inset here at the right. And this large signal is the far field signal and then these low amplitude signals, one of these is the local potential that we were actually capturing. And that's how we knew that this site was in the isthmus about 180 milliseconds proximal to the re-entry circuit exit. And when we ablated at that site, tachycardia terminated promptly. Now you can also appreciate from consideration of this electrogram, what would your mapping system have selected for activation at this site? Well, without editing, it likely would have selected this large sharp far field potential. And that could have created a misleading activation sequence map. And these far field potentials are a source for misleading activation maps. So entrainment offers the advantage that it doesn't require recording from multiple sites to determine the relationship of the pacing site to the re-entry circuit. You don't have to do a complete activation map. And even for hemodynamically unstable tachycardia, sometimes you can do this with just inducing tachycardia, a quick run of pacing, and then burst pacing to terminate tachycardia. If you need to determine is this area anywhere close to the re-entry circuit or are we miles away and off base? Pacing that captures indicates that your catheter is resting on viable myocardium that would be a potential target for ablation and not dense scar or that the catheter is simply not in contact. The problem with these pacing maneuvers is that they require a stable tachycardia and pacing may terminate the tachycardia or accelerate one VT to another ventricular tachycardia. Although if you pace just 20 or 30 milliseconds faster than the tachycardia with syncing the stimulator so that the first pacing stimulus falls late in electrical diastole when possible, that reduces the likelihood of these undesirable pacing effects. Now, so far a lot of the examples that I've shown you in the schematics suggest that the re-entry circuit is fixed, that we've got these areas of fibrosis that form fixed regions of conduction block. And that can be true, but we know that certainly in animal models, in the five-day-old infarct animal models, most of the re-entry circuits that you see are functional in nature. That is, that there are areas of conduction block that are determined not by fixed fibrosis, but by very slow conduction of the wavefront or areas of collision. And this is from an animal model from a nice publication by Elad Anter that shows you a functionally determined re-entry circuit. And when I play this video, you'll see that there's a wavefront that propagates through this isthmus from top to bottom. But if you look carefully, you'll see that there's propagation that's also occurring from the middle portion of the isthmus out towards the right and towards the left. And these very slowly conducting wavefronts that are going perpendicular to the long axis of the isthmus collide with wavefronts from the outer loops. And that defines this double loop type of re-entry. So here it goes. We'll see activation through the isthmus, and then you can appreciate there's left to right and right to left propagation in the isthmus with the exit at the top and the entrance at the bottom. So Dr. Anter has studied entrainment responses in this kind of a functional model and shown that it agrees quite well with predictions from more fixed type of re-entry circuits. But the thing that he did notice is that in the exit region that you can have entrainment responses that suggest that you're in the exit of the isthmus when you're in fact outside of the isthmus, a little bit beyond the exit from the true exit from the isthmus region. And you'd expect you'd have relatively short stem-to-QRS intervals during entrainment here, but can still have entrainment with concealed fusion and a post pacing interval that indicates you are in or near the re-entry circuit. And this again from his publication just makes the point that you see these abnormal electrograms in the isthmus region, but can also see them in bystanders and in the outer loops. And the entrainment responses are consistent with what we would expect from the anatomically considered re-entry circuits. Now entrainment mapping then is complementary to activation mapping and here's a nice example of an epicardial re-entry circuit. So you see that we've got a nicely defined isthmus and then two loops. Note that the color coding of the activation sequence here is again not what you would necessarily expect. The entrance area is really color-coded as red and that just relates again to the timing of our fiducial point and activation window. Now let me just show you some of the entrainment responses from different points in this circuit. So at the top here we're entraining from the isthmus. We have entrainment with concealed fusion with a stimulus to QRS of 180 milliseconds, suggesting that the conduction time from this site out to the exit of the circuit is 180 milliseconds. Tachycardia cycle includes 500 milliseconds and that would land just proximal to these little low-amplitude electrograms and we can see that during pacing we don't see those signals here. So this could be the local potential. You can see that there's another very fractionated potential here but that potential is present during pacing. So this is a far-field potential and we did not measure the post pacing interval to these far-field fractionated potentials. In the lower panel you can see that we're pacing closer to the entrance region of the circuit. The stimulus to QRS is longer and the pacing stimulus falls within the preceding QRS complex. Again the post pacing interval indicates that we're in the re-entry circuit and there is entrainment with concealed fusion. Here is pacing in this loop around the outside of the circuit. Again the stimulus here falls in the end of the QRS complex. The subsequent QRS complex is entrained without fusion and this really looks like there's minimal fusion although if you look carefully I think I could argue that the QRS morphology is a little different immediately after the QRS complex here in these precordial leads compared to during tachycardia. In order to convince yourself that there's fusion here it can be useful to pace a little bit faster and show progressive fusion but this is in an outer loop area as the loop is approaching the entrance to the re-entry circuit and ablation in the isthmus terminated the ventricular tachycardia. So in summary entrainment can define the relationship of the pacing site to a re-entry circuit. There are many potential caveats and pitfalls to interpreting the entrainment mapping data. Combining entrainment mapping with activation mapping is a very powerful tool for guiding ablation of scar related re-entrant arrhythmias. And here are a couple of references that summarize much of what we've discussed. Thank you.
Video Summary
This video discusses the principles of entrainment for ventricular tachycardia (VT) mapping. The speaker explains how activation maps created with modern electroanatomic mapping can show examples of reentry circuits in scar-related reentry. The reentry circuits often take the form of a double loop or figure-eight circuit, with a wavefront emerging from an isthmus and propagating in counterclockwise and clockwise directions around the isthmus. These circuits form in areas of scar. Entrainment mapping allows clinicians to recognize parts of the reentry circuit and determine if the site is at a narrow isthmus where ablation can effectively interrupt the VT. The post-pacing interval, which reflects the conduction time to and from the circuit, can help assess the proximity of the pacing site to the reentry circuit. Fusion, which is a reflection of how the stimulated antidromic wavefronts can propagate away from the pacing site, can distinguish an outer loop site from an isthmus site. The speaker emphasizes that entrainment mapping is complementary to activation mapping and can be a powerful tool in guiding ablation of scar-related reentrant arrhythmias.
Keywords
ventricular tachycardia
entrainment mapping
activation mapping
reentry circuits
scar-related reentry
double loop circuit
figure-eight circuit
ablation
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