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Hypertrophic Cardiomyopathy: EP Considerations
Catheter Ablation of Ventricular Arrhythmias in HC ...
Catheter Ablation of Ventricular Arrhythmias in HCM (Presenter: Usha B. Tedrow, MD, MS, FHRS)
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Video Transcription
Good morning, everyone. We're going to talk a little bit about catheter ablation for ventricular arrhythmias and hypertrophic cardiomyopathy. And this is a little bit of an extension of some of the topics we've been discussing already this morning. So I'm going to begin by quoting some of the data from some of my colleagues that I presented to you earlier this morning. Looking now at the folks in whom we've already put an ICD. So the question is, how frequent is ventricular tachycardia in our patients with hypertrophic cardiomyopathy? And in this Tufts UT Southwestern collaboration, they found that of the ICD recipients they looked at, about 64% had evidence of non-sustained VT. And predictors of sustained ventricular arrhythmia requiring ICD therapy included the length of non-sustained VT greater than 7 beats, faster runs of non-sustained VT greater than 200 beats per minute, and repetitive runs of non-sustained ventricular tachycardia. In a separate publication, they looked at this phenotype of the left ventricular apical aneurysm, which was 4.8% of their total, 93 out of nearly 2,000 patients. And the sudden death rate was elevated in this group. But importantly, this group had a lot of monomorphic ventricular tachycardia that was sustained, requiring greater than two ICD shocks in 14%. And they had often to undergo VT catheter ablation to control recurrent ventricular arrhythmia. So what type of VTs are typically present in hypertrophic cardiomyopathy? At some point in the past, it used to be thought that there was very little sustained monomorphic VT in hypertrophic cardiomyopathy. But as we appreciate more and more that there is a fibrotic process that's part of hypertrophic cardiomyopathy, we've appreciated that scar-related reentry, just like what we see in other forms of structural heart disease, can occur in hypertrophic cardiomyopathy. So when we've looked in the past at folks that were referred for VT catheter ablation that have hypertrophic cardiomyopathy, we found that the majority have scar-related reentry, though automatic foci, such as the right ventricular outflow tract, the left ventricular outflow tract, and importantly, the papillary muscles, which can be quite thick, can also give rise to monomorphic VT. The reentry substrate can be endocardial, epicardial, or intramural. And I've just shown a little diagram for folks to look at how we think about these scar-related VT patients. When they have monomorphic VT, what we think of is areas of fibrosis with surviving myocytes. And the surviving myocytes have poor cell-cell coupling, and some coupling with some of the fibrosis nearby that creates slow conduction. And there can be circuits that form within the scar. And you can see how they could potentially be intramural, particularly if the wall thickness starts to be very great. So in referral populations now, there have been several studies published over the years looking at patients with drug refractory VT and hypertrophic cardiomyopathy undergoing catheter ablation for VT. And up to 80% have demonstrable epicardial low-voltage substrate. So when we move a catheter around the epicardial surface of the heart, we find low voltage. And this population of HCM patients more often have a reduced ejection fraction. They may be at a very late stage in their disease. But there are those in whom their LV function is preserved. The majority of the scars that are observed are septal, involving either the base or the apex. But they also can have periaortic and perimitral scars like what we're used to seeing in other forms of non-ischemic cardiomyopathy as well. And this is just an example to let you know what the type of scars can look like and why they're so hard sometimes for us to detect with our catheter. Here's the interventricular septum. And you see these little patchy scars here. And you imagine if I'm moving my catheter across the endocardial surface here, I'm going to encounter mainly normal tissue. I may not be able to discern the fact that there's any kind of low voltage or abnormal tissue there. So adjunctive imaging in the future is going to be very important. Historically, to date, it's been very challenging because this area of the heart is very hard to image in folks with defibrillators, even with contrast CT preparations to try to detect the scar. And sometimes these scars are very small. The other thing I'd like to point your attention to is this papillary muscle that you can see here that has a tremendous amount of fibrosis within the papillary muscle itself. And we know that little bits of Purkinje tissue live in the papillary muscles and can, in conjunction with the scar, end up with automatic VTs from these types of structures. So those are the kinds of pathophysiology that we're thinking of when we think of these patients with VT. And I'd like to show you here the results of a relatively recent publication from the International VT Consortium, which is a group of quaternary referral centers that perform a lot of VT catheter ablation. It's basically all of us pooling all of our complex cases together. And Marmar Vesaghi from UCLA has recently been the lead author on this publication of the outcomes of all of our non-ischemic cardiomyopathy patients undergoing VT catheter ablation. And what you can see is the black line here is the hypertrophic cardiomyopathy. You have VT recurrence here on the y-axis and then follow-up. And you can see just shy of the sarcoidosis patients that have terrible recurrent monomorphic VT. The hypertrophs are just behind there. So it's a very challenging group of patients. And you see that they're here as well when you look at adjusted VT recurrence, death, and transplant by etiology. You see the hypertrophic cardiomyopathy patients are a big challenge for us. In addition to the success problem that we have with the hypertrophic cardiomyopathy group, I respect them a lot in their capacity for instability during invasive procedures. So I think we all need to think about them with a lot of trepidation when we're taking them to the lab if they're having VT storm. It's a different kettle of fish from when we're taking them for atrial fibrillation ablation. I think they're at a very different stage in their disease. But these folks that have reduced ejection fraction who may have an apical aneurysm, we need to make sure we screen them for a possible endocardial LV thrombus. We need to make sure their heart failure regimen is optimized as much as possible. And I think these are the patients that are sick enough that we need to sit down as a team and figure out what our plan is. If we can't get out of dodge, are they an LVAD candidate? Are they a transplant candidate? What do we want to be thinking about for the future of this patient? Because our goal is usually to stabilize them, but we'll want to know what they're headed for in the future. We also need to plan based on the VT morphology often what our best approach is to the ventricles, whether we're going to go retrograde aortic, whether we approach the ventricles transeptally, epicardially, or with other adjunctive therapies. We need to have an anesthesiologist that understands the physiology of hypertrophic cardiomyopathy, particularly for the patients that still have obstruction. I think it's very important that if a patient's going to be under general anesthesia for a big ablation procedure that they're not run too dry. If they happen to have a complication where they bleed, they can have a real problem with their outflow tract obstruction getting augmented by the reduced filling, which is a real problem. So I just want to show you a couple still pictures from an ablation of a patient with an apical aneurysm. And I think that the maps that we create in these folks almost look comical. It looks like there's almost no cavity here. So this is the left ventricle. This is the mitral annulus here. And this is the body of the left ventricle coming out into this left ventricular aneurysm down here. The scar in these apical aneurysm patients is often located down at the apex, just like this. And you can see here, this is an intracardiac echo picture, where we're looking from the right ventricle over to the left ventricle, how thick the free wall is. You can see centimeter markers there. And how tiny the cavity is. And that's emphasized here, too, when I change my ultrasound slice to look more longitudinally down the left ventricular length towards the apex. This is the apex here. There's a tiny channel going from the base to the apex. And this is one of the reasons that I like to approach these patients from a transeptal approach, because you can steer the approach of your catheter a bit better sometimes than you can retrograde aortic. But sometimes it's a challenge just to get your catheter down into this aneurysm area. The VTs that we see from these patients are very predictable. They usually have two VT morphologies. One that exits out the lateral part of the scar, going this way. And one that exits out the septal part of the scar. And they often have a channel that goes through the middle. And so this is an example from this patient where you can see it's very negative in LEAD-1, which means it's exiting out more laterally. And you can see it's very negative in V3 through V6, which puts it extremely apical, which is not a big surprise. But then the other VT morphology is just a little bit narrower. It's a little bit more isoelectric in LEAD-1. And so that one is exiting more septally. And what we'll often see when we get a catheter down in that apex is that if you pace in sinus rhythm, you see different stimulus to QRS times with the different morphologies that you're able to see during VT. So you often see this, and you try to ablate it. And you can render the patient non-inducible, and you think you're great. But they recur then within a few weeks, typically, because the tissue is so thick. So in this particular patient, I used a strategy where you use half-normal saline irrigation to enhance the size of my ablation lesions. And that was able to keep this patient non-inducible. But oftentimes, what we'll see, this is just a little more data from our series of the patients with these apical VTs. And you see a very, very similar QRS complex from what we just saw in the example. But what we'd had to do in a lot of these patients where something like half-normal saline doesn't work is you have to do epicardial access. And you can identify the low-voltage scar at the apex. This is just shown in a couple different views. And so you ablate on the endocardium and on the epicardium in hopes of getting block through that very thick tissue. Another common morphology that we see in our patients with hypertrophic cardiomyopathy is more of this sort of lateral basal morphology. So this is a right bundle VT that's positive concordance throughout the precordium. And that's way up at the base of the heart. And it's a bit lateral. It's starting negative in the lead AVL. So it's way over towards the lateral part of the mitral annulus. This is a shell created by the ultrasound here. And what you can see is the site where we mapped this VT. And the ultrasound here, this gentleman, his lateral wall of his heart was more than 2.5 centimeters across, one of the largest we've ever seen. We ablated with a standard catheter, and nothing happened to his VT. We went on the epicardial surface and ablated out here, and nothing happened to his VT. So we had to do something more dramatic. And so we've been doing some cases with an irrigated needle catheter. And this is just a plot of some of the animal data that's been done with the needle catheter shown here in green. This is depth of the ablation lesion and cross-sectional area. This is a standard ablation lesion that's able to go six millimeters into the tissue at best. And with an irrigated needle, you can achieve lesions that go as far as 16 millimeters into the tissue. And so that's what we did for this patient. This is an example of the needle that's been deployed into the myocardium. And it slowed the VT down and ultimately terminated it. Now the end game of this particular patient was not as good, because he did recur again after six months, despite even this intramural ablation that we did. And he actually had to go for an open chest surgical ablation. And he's now been without VT for about six months. So we'll have to see how he does down the road. But they're very, very difficult cases, because the heart muscle is so thick. So just in summary, I'd like to mention that monomorphic VT is uncommon in hypertrophic cardiomyopathy. But when it happens, it can be really bad. And we need to be prepared for how we're going to manage people when they have it. It's an important source of both morbidity and mortality. It requires a team approach to managing the patient both before and after the procedure to make sure that they get through OK without having hemodynamic problems. Small thickness and intramural scar are important barriers to durable and successful ablation. And adjuvant strategies are often required. Thank you very much for your attention. OK. All right. One question. I guess the ventricular tachyarrhythmias and HCM are reentry predominantly. Is that your point? Sorry. Say that again. I can't hear over there. The ventricular tachyarrhythmias and HCM are reentry predominantly. OK. Can't hear over there. So ventricular tachyarrhythmias are largely reentry mechanisms, right? What about the old idea of the disorganized cells, of course, something we can't validate directly and all that? Do you think those gap junctions, could that be a mechanism as well without scar? So the question is, can you see ventricular tachyarrhythmias without fibrosis as the pre... And I think that's true, that there's definitely a population of folks, particularly when we looked back at our ablation series and looked at the apical hypertrophic cardiomyopathy patients who don't maybe have so much fibrosis. There was a much higher incidence of normal RV outflow tract tachycardias, which are probably not a risk for sudden death in those patients. OK.
Video Summary
In this video, the speaker discusses the use of catheter ablation for ventricular arrhythmias and hypertrophic cardiomyopathy (HCM). The speaker presents data from studies that show the prevalence of ventricular tachycardia (VT) in patients with HCM, as well as the predictors for sustained ventricular arrhythmias requiring treatment. They also explain the different types of VTs that are commonly seen in HCM and discuss the challenges in detecting and treating these arrhythmias. The speaker emphasizes the importance of a team approach in managing these patients, particularly those with reduced ejection fraction and apical aneurysm, and highlights the need for adjunctive imaging and careful planning for catheter ablation procedures. Additionally, they present case examples of patients with HCM and discuss the difficulties and potential strategies for ablating these arrhythmias. Overall, the speaker emphasizes that while monomorphic VT is uncommon in HCM, it can have significant morbidity and mortality, and a multidisciplinary approach is crucial for successful management.
Meta Tag
Lecture ID
6712
Location
Room 152
Presenter
Usha B. Tedrow, MD, MS, FHRS
Role
Invited Speaker
Session Date and Time
May 09, 2019 10:30 AM - 12:00 PM
Session Number
S-012
Keywords
catheter ablation
ventricular arrhythmias
hypertrophic cardiomyopathy
ventricular tachycardia
sustained ventricular arrhythmias
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