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Ventricular Tachycardia: The Cause Is the Key to Management

The heterogeneity in ventricular arrhythmias shouldn’t be overlooked when planning chronic management for a given patient and deciding whether an implantable cardioverter-defibrillator (ICD), antiarrhythmic drug, or catheter ablation would be appropriate therapies.

In this episode of the AP Cardiology podcast, Andrew Perry, MD, speaks with Melissa Robinson, MD, of University of Washington, Seattle, about three cases that illustrate why there is no one-size-fits-all approach to ventricular tachycardia.

A transcript of the podcast follows:

Perry: Hi everyone, Andrew here. For this episode, I have a fantastic educator visiting. Dr. Melissa Robinson is a star faculty at the University of Washington in the electrophysiology section. She focuses on complex ablations. She is the go-to person for complicated patients and does a lot of the ventricular tachycardia ablations. She is well known among her colleagues for being meticulous, methodical, and very attentive to her patients. I spoke with her about ventricular tachycardia over three cases that demonstrate the heterogeneity of this arrhythmia. I learned a lot preparing and discussing these cases, and I think you will too. With that, let’s get started.

This is AP Cardiology and this is your host, Andrew Perry. Thank you for meeting with me today, Dr. Robinson. May I have you give your name and your title for our audience so they can get to know you?

Robinson: Sure. I’m Melissa Robinson and I’m an associate clinical professor at the University of Washington. I’m the medical director of the electrophysiology lab, but what I’m most passionate about is I’m the director of the complex ablation program, which encompasses ventricular arrhythmias and arrhythmias in adult congenital heart disease.

Perry: Perfect. Thank you. Leading off utilizing your expertise, I’ve prepared some cases to discuss ventricular tachycardia, and we’ll be focusing our discussion on more of the chronic management of ventricular tachycardia since the acute management of ventricular tachycardias is well outlined within ACLS algorithms.

Robinson: Sounds good.

Perry: We’ll just launch right ahead and go with our first case. We are seeing a 48-year-old man who’s obese with diabetes and during his lunch hour at work, out at a restaurant, he has a cardiac arrest. EMS is quick to arrive to the scene and they find the patient in polymorphic ventricular tachycardia, and he’s treated with successful defibrillation.

The post-cardioversion EKG demonstrates an anterior STEMI, and he’s taken to the closest cath lab where he’s found to have an acute occlusion of the proximal left anterior descending artery and undergoes a successful PCI to that artery. Because of the out-of-hospital cardiac arrest, he was initially cooled because there was no initial neurological recovery, but eventually regains neurological function and is recovering well in the hospital.

We’re seeing him at the time a few days after that initial event and on his telemetry we’re seeing some shorter runs of non-sustained ventricular tachycardia that have been more present closer to the time of the event, but have been decreasing in frequency throughout his hospital stay. As we’re thinking about this patient, and the question often comes up about whether this patient needs or would benefit from an implantable cardio defibrillator, or an ICD. What are your thoughts about that?

Robinson: These are dramatic events in patients’ lives. This was a public arrest and so this often gets folks thinking that they really need dramatic therapy above and beyond the stent. But there’s actually quite a bit of data because cardiac arrests due to acute myocardial infarctions are not all that rare, frankly, and so we’ve been able to study this group. There is a lot of data from randomized trials that support just revascularization and goal-directed medical therapy for this particular patient.

One thing that’s interesting is you’ve left out the ejection fraction in the stem of this case and I think there’s a point to that. It actually doesn’t matter what the ejection fraction is in terms of our current guidelines. Even if the ejection fraction is low in this instance, he has had an acute myocardial infarction and the initial therapy is simply revascularization.

Perry: Perfect. Now, does that change at all in terms of patients who are having salvos of non-sustained ventricular tachycardia? Sometimes we see those patients and we get nervous that they’re having a lot of ectopy and whether they are at greater risk for having another event, maybe another event of ventricular tachycardia.

Robinson: Yeah. Right. I do think that you really put the nail on the head that we do get nervous, so some of the things we do are treating the doctors. I think this really is a role for an electrophysiologist to help out the CCU team, and the cardiology team, because there are sort of different flavors of non-sustained ventricular tachycardia. If this patient is having PVCs that are initiating somewhat polymorphic-looking ventricular tachycardia, I’d actually be a little bit worried that he’s under-revascularized… that’s not a word [LAUGHTER]… but that we haven’t had full revascularization and that there is ongoing ischemia.

It does matter where the ischemia is, so the His-Purkinje system, the left anterior fascicle and especially the left posterior fascicle, which seems to get disconnected from its blood supply a little bit easier. The left posterior fascicle tends to be really irritable in an ischemic environment and these areas can trigger off ventricular fibrillation. We don’t really know what this patient’s presenting arrhythmia technically was. Did he have a monomorphic VT that went on for long enough and it degenerated? Did he go straight into polymorphic VT? We don’t know.

Ischemia-driven arrhythmias tend to be more polymorphic, less regular, less dependent on sort of preformed circuits within preformed scar and related to heterogeneous conduction, heterogeneous repolarization within a larger mass of ischemic muscle, so they tend to be sort of uglier.

If this gentleman’s having non-sustained VT… some of these patients will even have non-sustained monomorphic VT coming from the outflow tracts, which is just sort of an adrenaline-driven area that we can see even in normal hearts. That would make me less worried about this particular patient, so I do think the morphology matters and how you localize it onto the substrate that you’re dealing with, where was the infarction?

Perry: Okay. Just to summarize, having runs of non-sustained ventricular tachycardia in some situations may make you more concerned to perhaps escalate therapies for that patient, but there may be other forms or in the morphology of that non-sustained ventricular tachycardia, that NSVT, really would have a large sway in your clinical decision making for a patient like this, who presumably his VT is purely ischemia-driven.

Robinson: Yeah. I would agree with that. Frankly, if you look in our guidelines, really, non-sustained VT is not an indication for ICDs. It’s not really in any substrate outside sort of chronic substrates like the genetic cardiomyopathies and things. It can be one more risk factor. But in an ischemic cardiomyopathy patient, post-MI patient, non-sustained VT doesn’t actually come into the algorithm.

Perry: Okay. Perfect. Let’s fast-forward this same patient at 18 months later, and so he had a revascularized LAD STEMI. Now at home, he has a VT arrest at home. Again, 911’s called and EMS arrives, and this time their strip demonstrates a monomorphic ventricular tachycardia. He gets successful defibrillation and he’s brought to the hospital. His post-myocardial infarction ejection fraction was around 45% and currently at home his medications, relevant to this discussion, I think, are a statin, metoprolol, aspirin, and clopidogrel.

When he is admitted, he has some mild troponin elevation, but not like a dramatic rise and fall that we’re concerned about having an acute coronary event, but he’s still taken to angiography and demonstrates a patent stent in the LAD and with stable, non-obstructive coronary disease in the right coronary artery and in the circumflex. Now think about this patient later on, in a situation where we’re thinking not so much ischemia-driven. But the initial event 18 months ago was all from ischemia. Is this a patient who now would benefit from an ICD and maybe what’s changed if so?

Robinson: I think this is really an interesting scenario. #1, you have a patient who has had a myocardial infarction and has chronic LV dysfunction, but it’s relatively mild, so by all of our current criteria he did not meet indications chronically for primary prevention ICD. His ejection fraction was 45%, and you didn’t say it, but we’re assuming that he wasn’t having heart failure symptoms. He doesn’t get an ICD, but then he still is a patient who presents with sustained VT and has a cardiac arrest, so now this patient meets secondary prevention criteria.

This did not happen within the setting of a new myocardial infarction and this happened in the setting of, presumably, some healed scar, so that substrate’s not going away. Even if they’d gone in there and done a little balloon angioplasty and some in-stent restenosis, this is monomorphic VT that lives within sort of chronic remodeled scar. They tend to present years after the initial event, but can present as soon as even three months after a larger myocardial infarction where we’ve had a lot of injured muscle. You know that even though he was revascularized he clearly created some scar.

His ejection fraction is abnormal and as an electrophysiologist I like to go sort of one step further. His EF is 45%, but does he have a focal wall motion abnormality? Is this consistent with the territory we’re looking at? Does he have an anterior septal wall motion abnormality?

Because then it all fits. That’s the area that didn’t get enough blood, that’s the area that created scar, and that’s where we probably had some re-entry within the scar, so electrical circuits were spinning around within those corridors in the scar and creating monomorphic VT.

He definitely needs an ICD. It’s not enough to put this man on antiarrhythmics. That’s been shown very clearly in secondary prevention trials that are, honestly, older than perhaps many of the listeners to this podcast. The question, really, is, “Should he get an antiarrhythmic along with his ICD?” That’s a little bit dealers’ choice at this point.

Some people would even say he potentially could come to the electrophysiology lab and get a catheter ablation. We have very few randomized trials of catheter ablation in ventricular tachycardia patients and one of them is a trial called SMASH-VT that was done about a decade ago. Vivek Reddy is the senior author on that and a lot of the cases were done in Europe and Prague. They took patients just like this who met indications for an ICD in the setting of ischemic cardiomyopathy and had had monomorphic ventricular tachycardia, and they randomized them to defibrillator versus defibrillator and ablation. The folks who got sort of a prophylactic ablation, if you will, it was their first episode, they had fewer ICD events.

They can’t seem to show mortality benefit in this population, so I think that we’re sort of chipping away and adding therapy, not necessarily life-saving therapy beyond the defibrillator, but we can add to this patient’s course by decreasing their overall events. Most patients in clinical practice will get the defibrillator alone. Some of them will get some antiarrhythmic. In the rare patient, it may make sense to go straight for ablation, depending on how much information you have, the 12-lead EKG etc.

Perry: This patient is already on metoprolol. Do you think there would be any benefit to trying to increase that to like a maximally-tolerated dose sort of approach, as that can be somewhat of an antiarrhythmic in terms of ventricular tachycardia?

Robinson: It definitely can be, but the data’s modest, and so much of the data for treating ventricular tachycardia with metoprolol is like 30 years old and it’s really a pre-revascularization era. Certainly, we didn’t have more modern aldosterone inhibitors, ACE inhibitors, all of the fancy drugs we have now for ischemic cardiomyopathy.

They quickly moved into the formal antiarrhythmics, sotalol, amiodarone, which have been shown to decrease ICD events and decrease VT events in patients with ischemic cardiomyopathy.

I don’t push the metoprolol dose too hard. I sometimes will see patients that… I just did an ablation this week on a gentleman who was on 100 bid of metoprolol. He’s 72 years old. He’s dizzy all the time and tired, so I do think that pushing the metoprolol too high really doesn’t pan out. That being said, we probably underdose a lot of patients, even if you’re looking at the primary heart failure literature, so it’s not unreasonable to go up on that dose as a first start.

Perry: Some maybe like summative comments about this case. Because when we see this patient 18 months later after another event of ventricular tachycardia, and as you’ve mentioned, this thought or concern that with our “retrospectoscope” say, “Well, this patient had another event and have we done this person a disservice by not treating them more aggressively like with a device or possibly antiarrhythmic therapy upfront at the time of the initial STEMI?”

But I think, as you’ve well discussed, that there is really no data for those approaches, at least as of yet. I don’t know if there is other active research in trying to delineate who are these patients who may go on to develop scar and then scar-based ventricular tachycardia versus those who recover from their MI without, who are then lower-risk for VT in the future.

Robinson: Yeah. I think these kinds of studies, this is really the sort of promise of big data, so healthcare systems in Europe, and there are a lot of places like the Netherlands and other countries that really keep sort of uniform healthcare data — Canada does a pretty good job about this — where the healthcare systems aren’t as fractionated and they can really keep large population databases and get the patients’ echos, get the patients’ EKGs.

I really do think that machine learning and taking a deep dive into large datasets is going to help us with better prediction models. Even 700, 1,000-person studies where we randomize these kinds of patients to therapies I don’t think are going to pick out the patients who will actually benefit. Because a 49-year-old man who had an anterior wall MI and has an EF of 45% with diabetes and obesity, those can be very heterogeneous patients in terms of arrhythmia risk. It really comes down to substrate and the intermix between the autonomic nervous system and substrate. It starts to get a little nuanced, frankly, but it speaks to how difficult it is to predict these things, and to have guidelines that are currently just essentially based on ejection fraction feels very unsophisticated because it frankly is, and we know that.

There is really cool MRI and computer-based modeling within scars to predict which scars are actually arrhythmic, really neat stuff that I think isn’t ready for primetime, wide distribution. It’s expensive and it’s laborious, but I think that… I hope in the next 5 to 10 years that we’ll be doing more kind of personalized medicine to say, “Hey, this person’s at risk.” But certainly within standard of care, nothing was amiss on this particular patient and him presenting with monomorphic VT related to his scar 18 months later is not the same thing as his polymorphic VT at the time of the occluded artery, and they don’t predict each other. Obviously, the monomorphic VT doesn’t predict retrospectively, but the polymorphic VT does not predict monomorphic VT. The vast majority of those patients will do fine and I have a lot of patients in my practice who I saw after these kinds of events as a second opinion, “Hey, I’m worried I need a defibrillator.” Or, “I don’t want a defibrillator and the doc wants to put one in.” They do fine for years and years and years.

Perry: Interesting stuff. Okay. Let’s move on to our second case here. Now, we have a 60-year-old man who has a history of idiopathic dilated cardiomyopathy who has a chronic ejection fraction, around 30%. He is currently doing very well with New York Heart Association class 1 symptoms and had a primary prevention ICD placed some years ago because of this reduced ejection fraction.

He has a syncope at home and received a defibrillation from his ICD. He quickly regains consciousness. His wife calls 911 and he is brought to the hospital. A device interrogation demonstrates a monomorphic VT that was unsuccessfully treated with anti-tachycardia pacing and then was successfully defibrillated. His current medications include lisinopril, carvedilol, and spironolactone. The initial labs are notable for a potassium of 3.0 and a magnesium of 1.7. On first approaching this patient, how do you approach this patient’s ventricular tachycardia and how to manage it?

Robinson: Yeah. I think this is a pretty common case, actually, for us who follow folks with ICDs. The initial management is really a deep dive into the event itself, so making sure that this was a monomorphic VT on the device interrogation, like you said, and seeing how it may have started. Sometimes these are starting because the patient’s having frequent PVCs and if you’re seeing that then you may want to direct therapy at the PVCs such as antiarrhythmics, and then really looking at the anti-tachycardia pacing, the ATP.

This kind of gets ahead of us here, but not all ATP is created equal and there are sort of nominal settings on how much faster the anti-tachycardia pacing is in relationship to the ventricular tachycardia. The concept here is there’s a circuit in the heart that’s running around and if we can just get slightly ahead of it we can depolarize the tissue in a way that makes it refractory when the arrhythmia spins back around and it terminates itself, sort of a dragon catching its tail, so to speak.

You want to pace ever so slightly faster than the tachycardia. But if you’re only a little bit faster, it won’t stop it. If you’re too fast, it can degenerate it into ventricular fibrillation, and so I always like to look at the shocks, what actually happened, and see if I can modify the anti-tachycardia pacing. Can I pace it a little faster if it didn’t work because it wasn’t fast enough? Can I try a couple more times? There’s a lot of nuance that we can go about and I do think tailoring it to the patient’s individual events is reasonable. There’s frankly no data to support that, though. This is a hard thing to study.

Perry: Okay. Yes, I was interested in that in particular because I feel like if you’re implanting an ICD for primary prevention you’re just kind of picking these ATP settings from probably whatever the default setting is from the manufacturer and leaving it at that, I would guess?

Robinson: Honestly, for the most part, that’s fine. A reasonable amount of modeling has gone into this. We sort of forget when we’re on the physician and practitioner side that there is a lot of scientists really working really hard on modeling and thinking about this to help us take care of patients, so their nominals aren’t totally random. They really are based on lots of simulations and collated data from thousands of events, so they’re totally reasonable. But you can then see how they interacted with the patient’s particular substrate. If every time a patient gets ATP it accelerates it into ventricular fibrillation, wow, you need to change something.

Perry: All right. Got it. Yeah. Okay. Before we get into further discussions of management, actually take one step back. This patient is presenting with ventricular tachycardia, with reduced electrolytes of a low potassium and a slightly low magnesium. I want to get your thoughts on you how you approach patients with electrolyte abnormalities who then have ventricular tachycardia, and when you consider those electrolyte abnormalities to be causative for ventricular tachycardia.

Robinson: Now I think those are really good points. I do think that electrolytes matter, so I do have several patients who take magnesium in particular because magnesium will help you hold onto potassium and it does seem overall to decrease their episodes. But for the most part, these electrolyte abnormalities that you see on presentation self-correct. They have to do with the shock itself with adrenaline surges and you can actually get a drop in serum electrolytes related to the actual event itself in sort of mysterious ways, if you will.

Unless this person has a reason like new diuretic therapy, some endocrine abnormality where they may be potassium-wasting, I think you should assume that they’re not running around just randomly with a potassium of 3. You can go back and look at their other labs that were done in other contexts that this probably isn’t just provoked with electrolytes, and this doesn’t end up being a primary target for us. The overwhelming majority of folks who present with an arrhythmia are going to have normal electrolytes. They happen sort of in the outpatient setting, so it’s not a primary target for me.

Perry: Okay. Then one last question on that is we’re taught more classically that electrolyte abnormalities result in polymorphic ventricular tachycardia rather than monomorphic VT. Your thoughts on that? True, not true, mostly true but often exceptions?

Robinson: Yeah. I think it’s mostly true, actually. If you’re truly hypokalemic or hypomagnesemic, then you’re going to prolong your QT interval. The real cellular basis of the prolonged QT interval is that you’re increasing the dispersion of repolarization, so the muscle cells throughout the myocardium are repolarizing at different times and that doesn’t generally set you up for re-entry.

Re-entry is really based on slow conduction, so muscle cell to muscle cell because there’s intervening fibrosis, or there’s a narrow channel, and so the actual conduction cell-to-cell is slow. But when you have repolarization that’s slow and heterogeneous across the muscle, you get polymorphic ventricular tachycardia and ventricular fibrillation. You get wavelet re-entry, these really small changing waves, and so that seems to be very true.

Perry: Okay. Back to our patient in terms of management. Anyone getting an ICD, that’s a traumatic event and a distressing event for patients. The ICD did its job in saving this person’s life, but there’s an emphasis on reducing the amounts of defibrillations that patients experience. One of the things in our armamentarium include antiarrhythmic drugs like amiodarone, sotalol, and others. What would your approach be in selecting an antiarrhythmic, or even if you would use an antiarrhythmic for this patient after their first episode of VT with a shock?

Robinson: I usually, with a shock, would end up starting an antiarrhythmic unless we really identified a reversible cause. They were in heart failure before the shock and we needed to get them out of heart failure. They were missing their medicines. They were sick, so COVID, other viral illnesses, UTIs and things can precipitate this. We’ll see this also postoperatively from things like gallbladder surgery or hip replacements because of the adrenaline surges.

If we don’t think this is a reversible event and if the patient doesn’t identify a behavior that’s a reversible event such as alcohol ingestion or something like that, then I do think an antiarrhythmic is warranted even after just a first shock.

Many patients are actually amnestic to their shocks because of cerebral hypoperfusion, thankfully, but most patients aren’t. The devices are a little bit of a quick trigger and these are traumatic events. We’re not giving antiarrhythmics just to treat the psychology of a shock, the trauma, if you will, but because ongoing shocks run the risk of one of them not being successful. Defibrillators are only so good at converting these arrhythmias and the more you have the more you’re sort of rolling the dice that one of the episodes might not be successful, or that it will be electrically successful, and the patient will be converted into a paced or sinus rhythm but have pulseless electrical activity, which we’ve all seen when we’ve done codes on the floors and things.

Perry: Sure. Yeah. Okay. I guess what would be the antiarrhythmic of choice in this patient? Just to review that, I think the salient points, younger 60-year-old man, non-ischemic, dilated cardiomyopathy.

Robinson: Yeah. antiarrhythmics really are a little bit limited in these folks, so we have a few options. We tend to not use the class Ic drugs, flecainide, propafenone, in structural heart disease. When there’s scar, and certainly in ischemic cardiomyopathy patients, these are no-no drugs. They have been shown to increase sudden death events in those patients, so we’re not going to use those.

It leaves, really, the class 3 agents, so we’ve got amiodarone, sotalol, and potentially dofetilide, which also has an indication in this setting if the patient’s not in active heart failure. Sotalol and dofetilide both require a fairly normal QT interval, and a corrected QT interval specifically, about 440 or 450 at max. This can be a little bit challenging if the patient’s QRS is already widened, either because they have an underlying bundle branch block or they’re paced, so there are kind of back-of-the-napkin corrections for this and they all kind of do it in a similar way where you’re essentially accounting for the excess depolarization time, the excess QRS width, and subtracting it in some form from the QT interval.

A lot of patients with cardiomyopathy have long QT and it makes these two drugs drugs we can’t use, and so that leaves amiodarone. Amiodarone is our most powerful antiarrhythmic, but that power comes at a cost in that 20% to 25% of folks on long-term amiodarone will have a significant side effect that will likely lead to its discontinuation, and that includes thyroid disorders. Luckily that’s usually hypothyroidism that we can treat, but can be hyperthyroidism, which is especially disconcerting in someone with ventricular arrhythmias, can lead to storm, and is not a good situation. Liver dysfunction thankfully is very rare, as is pulmonary dysfunction, but a lot of patients just don’t feel well on it and it’s sort of a head-to-toe drug. It can affect a lot of systems and so it is our drug of last resort, but frankly, I have quite a few patients on it to control the arrhythmias. I think in this patient I would be hopeful that I could put them on sotalol.

Perry: Okay. Aside from antiarrhythmic drugs, something that you do a lot are ablations for ventricular tachycardia. I’d be curious, kind of framed around the presentation for this type of patient, when do you consider referring this person for an ablation, performing an ablation? Is it something that after their first event, since he’s so young, just to avoid any toxicities from amiodarone if he’s not a candidate for sotalol, just to go straight for an ablation and try to ablate these PVCs or the focus of origin? Or do we maybe make some modifications, see how things go, and if he continues to have more, then refer for an ablation?

Robinson: Yeah. I think this is excellent and you sort of stopped yourself, but I’m going to point out that you started to say, “Do you put him through an ablation?” I think that’s been the sort of viewpoint of most cardiologists, referring cardiologists, and even electrophysiologists, that the burden, if you will, that the barrier to putting someone “through” a VT ablation has to be kind of high. It’s sort of my life’s work to lower that barrier for the patients who would benefit, like the prior patient is a reasonable patient to go through a safe procedure. This doesn’t have to be a 9-hour slog or an unsafe procedure.

That being said, this is a 60-year-old man with non-ischemic cardiomyopathy, and that is a very different animal. I focused a lot in the ischemic cardiomyopathy case that there’s substrate and that we’re looking at substrate in relationship to the coronary artery disease and we know where the scarring is.

This particular patient, you haven’t given us the details, but what do we actually know about his heart disease? The heart failure specialists really are moving away from that term “non-ischemic cardiomyopathy.” We’re trying to be more specific because the phenotypes, both from a heart failure standpoint and from an arrhythmia standpoint, they’re different based on the underlying etiologies.

I’m often referred this kind of patient after they’ve had more events on antiarrhythmics. I don’t think this is a patient who should go straight to the lab. I think they should be on an antiarrhythmic first and the guidelines would support that for a non-ischemic etiology.

But let’s say he had ongoing episodes. I get referred these patients by my colleagues to do their ablation and I may be the first person who is saying, “Hey, wait a second. Have we ruled out sarcoidosis?” For instance, “Have we ruled out really significant valve disease that we’re missing? Have we ruled out ARVC in this patient?” It’s not really… the R in the ARVC is going away.

This arrhythmogenic right ventricular cardiomyopathy really can be a biventricular process, and so have we sent them for genetic testing and this is lamin cardiomyopathy, which has a very different prognosis? I even get to diagnose Chagas disease every now and again, which is kind of a fun one, and that has a different trajectory. I like to step back and say, “What is the underlying etiology?”

But certainly within a non-ischemic population, these are folks that should be on antiarrhythmics before catheter ablation is considered and probably should have had multiple events, frankly, before they come for catheter ablation. The reason is the ablation is just not as successful in this population as we’d like it to be. It can be very helpful, but there is about a 50% recurrence rate at 2 years and it’s worse in some substrates.

Perry: Okay. But it sounds like that the success rate and thereby the threshold for referring to ablation is different in patients with ischemic cardiomyopathy.

Robinson: Definitely. Our endpoints and understanding of that substrate and ability to map that substrate, which tends to be sub-endocardial in ischemic disease, it’s a lot easier to go about those ablations generally. Epicardial substrate… I keep using that word, but I mean scar, and that’s really what we’re generally targeting with ablation. Epicardial scars tend to be… sorry, non-ischemic scars tend to be epicardial. They tend to be in the inferolateral wall, along the base of the mitral valve, perivalvular, and also in the mid-septum.

The middle of the septum is kind of an annoying place to reach with a catheter because our ablation lesions are only so deep and the septum’s fairly thick in a lot of these patients, preserved thickness, if you will, and we often just can’t reach it. I don’t want to say that we don’t do ablations in non-ischemics. We certainly do, but I think that they should have gone through other treatment pathways and that the treatment pathways aren’t as equivalent.

There is reasonable data in ischemic cardiomyopathy that ablation is similar to antiarrhythmic therapy and a lot of people will take that to mean we can just put the patient on drugs. Other people would take that to mean we can just take this patient for an ablation and have a similar outcome. But that’s not true for non-ischemics, so I do want to point that out.

Perry: Perfect. Thank you. Okay. Let’s move to the last case, kind of a different case from what we’ve been describing here. Now we’re having a younger woman. She’s 38, really no significant past medical history, and she presents to the ER and she’s been having palpitations and shortness of breath for about half a day or so.

She is found to have monomorphic ventricular tachycardia with a rate around 200, give or take, and a 12-lead ECG shows a right ventricular outflow tract morphology, which is not totally the purpose of our discussion here today, but we’ll just accept that at face value. She has received some IV metoprolol and the tachycardia is terminated.

She gets referred for a coronary CTA and that demonstrates normal coronaries. Her echocardiogram looks pretty normal and she goes for a cardiac MRI and this doesn’t show any fatty infiltrate in the right or the left ventricle. What’s your thoughts about…? How would you approach the risk in this patient in terms of having a fatal event from this person’s ventricular tachycardia?

Robinson: Now, I think this is a great case and really does give sort of the breadth of the heterogeneity in ventricular arrhythmias. This is actually not an uncommon situation, at least in my practice, I should say. We do see these patients quite a bit. The outflow tracts are really interesting. You’ve localized this to the right ventricular outflow tract, but the left ventricular outflow tract is definitely capable of this as well. The prognosis, if you will, and the manifestations aren’t felt to be all that different.

Embryologically, the outflow tracts are sort of the ends of the tube that then twists on itself, and so they actually are different muscle. They have different kinesin expression and different autonomics, and so this is an area of the heart that can create these automatic rhythms, so this isn’t scar-based VT.

These are renegade muscle cells, as I explain them to my patients, that can fire off. It tends to be adrenaline-driven, so it tends to be exercise induced. It can be caffeine induced, etc. and so some people will initially go after this as a lifestyle modification, so whatever they were doing to bring it on etc. I have a problem with that in that when you do monitoring on these patients they can have them during sleep. You obviously can’t modify your adrenaline levels during sleep. They can have them at other times.

I think it puts too much responsibility on the patient to control their own episodes and I see a lot of patients whose lives have kind of shrunk. They’ve stopped doing X, Y, and Z subtly over the years, and some of them have lost autonomy because their family members are nervous about their arrhythmia. I think there’s a lot to be said about lifestyle modification, but you have to make sure that the trade-offs aren’t too high.

This patient got the million-dollar workup. Outflow tract tachycardia is not an ischemic rhythm and certainly her pretest probability of having obstructive coronary artery disease at 38 years old as a woman was very low and would have been a red herring for this VT, and modification of coronary artery disease, if that was found, would not have altered this. The MRI is probably reasonable to get because you can have outflow tract tachycardia be the first manifestation of structural heart disease, namely arrhythmogenic RV cardiomyopathy, so I do think that that’s a reasonable thing to do.

I don’t do it in all of my patients, especially if I’m planning to come to the EP lab, because I can do some mapping during that case to help me decide if I think that they have structural heart disease. We can look for scar and if their echo shows a normal RV size and function, the possibility of ARVC goes way down.

Perry: Sure.

Robinson: Her first approach can be either a… honestly, if this is her first episode she can just watch and wait or she can try a medication, a beta blocker would be the initial choice or a calcium channel blocker, and a catheter ablation is also reasonable as a first option.

An ICD is not indicated here, okay? There are a couple of reasons. #1, the sudden death risk with outflow tract tachycardia is very low. There are case reports of sudden death and they tend to be monomorphic VT that degenerated into polymorphic VT, and they are very, very rare.

It seems to be that some of the publications have come out of Japan. I’m not sure that all of the same phenotype as what we’re describing here was represented in those publications, but it is not felt to be a sudden death syndrome. That being said, if you have monomorphic VT at 200 beats a minute while you’re driving a car you might not do so well, and so it depends on sort of the context for this individual patient how you will stratify.

But you can’t treat these patients with a defibrillator. The reason is that a defibrillator is going to see this ventricular tachycardia and it’s going to try and stop it either with pacing or a shock. When you get to the shock, what is that going to do? It may terminate the tachycardia, but it’s going to cause an incredible adrenaline surge and that’s going to put the patient right back into ventricular tachycardia, and the cycle will continue.

Frankly, it’s one of the most horrific things to see, even when I’m just looking at the strips without the patient in front of me, to know that this patient was literally tortured by their defibrillator. We don’t put defibrillators in for automatic rhythms, especially ones that are adrenaline sensitive, because they won’t stop.

It will just be incessant and it’s not a failure of the device. The device is doing exactly what you’re telling it to do. It’s a failure to choose the appropriate therapy within the appropriate context, so I honestly can’t emphasize that enough.

Perry: Gotcha. Interesting. That sounds like a horrific and very unpleasant event.

Robinson: And it’s difficult to regain the patient’s trust after that kind of thing too. Those are difficult situations, but these are lovely ablations. I just did one yesterday, honestly. These are accessible areas.

We can go after this in our cure rate for outflow tract tachycardia because you’re not dealing with heart failure. You’re not dealing with scar that’s changing over time. You’re dealing with a renegade muscle cell. Our cure rate is about 95% for these, so this is something where we can make it go away, it’s not looming over the patient’s shoulder, and they don’t have to take a daily medicine for very rare events that aren’t due to structural heart disease.

Perry: Okay. It sounds like for the outflow tract origin ventricular tachycardias, that there’s really a lot of leeway in terms of management, and maybe in part it depends on the patient’s risk tolerance. You’ve described driving in the car and then having a VT episode probably wouldn’t be pleasant. Maybe persons who are in higher-risk occupations like pilots or bus drivers or things of this nature may benefit more from aggressive therapy upfront to eliminate those episodes. But that maybe other persons, their risk for sudden cardiac death is low, their risk for any event is low, and so one initial strategy could be watchful waiting and then another management strategy can be trying beta blockers or calcium channel blockers, and then escalating to referring for an ablation later if these symptoms continue to persist.

Robinson: Yeah. I think that the early referral is also fine, because introducing the therapy to the patient, even if they decide not to go for it, is fine. A lot of the patients I see weren’t aware that there could have been a procedure and they take a medicine for five years, and I think we underestimate that. A lot of patients are interested in upfront procedures.

I want to lower that barrier a little bit for outflow tract tachycardia. These patients are often sent for cardiac catheterization if they come into the ER with this kind of presentation and there seems to be no barrier for that. But coming to the electrophysiology lab, which is also a catheterization of sorts, is not all that different, so it’s sort of how the patient views their health care.

A lot of patients will do anything they can to avoid a procedure. You will never have a complication of a procedure if you never have a procedure, so in those patients that’s not the right mentality. You have to have a particular situation where the doctor would really be pushing for that, so that you’re really concerned that their life’s going to be altered in a negative way. But other people, this is really how they’d like to take care of it.

Perry: Got it. Okay. Well, those are the cases that I had prepared. Maybe as some final thoughts or wrapping up, maybe I could ask you what are the things that really motivate you and things that you love about your job, and what you do in the care and management of patients with ventricular tachycardia, which I think is what a large part of your practice is?

Robinson: Yeah. When I was going into training, I was looking for something to sort of focus on and electrophysiology grabbed me early on. Then within electrophysiology it was very clear to me — within cardiology, certainly — that when someone’s in ventricular tachycardia everyone’s trying to figure out how to run away, so someone had to run towards those patients. I have sought out a training program to do this and so I’ve really built up a referral practice and a program around ablating VTs, so I see lots of sort of variance on the theme.

I think for me the biggest thing is making sure that wherever you practice, that your patients still have access to all the therapies. It doesn’t mean that everyone gets a catheter ablation, but that they have access to it. I do still get referrals that are really quite late, patients who’ve had 100 shocks and things like that. I think some of it is disparities of care and that’s such a part of the discussion now — socioeconomic, racial, gender discrimination — in terms of what we offer patients.

I definitely see it on the side of these kinds of procedures, and so keeping that in mind when we’re offering therapies to a patient and making sure that your patients have someone that you can refer for these kinds of things. An ischemic cardiomyopathy patient shouldn’t have to fail six drugs and have 25 shocks and have their life kind of really narrowed down before there is a consideration for a catheter ablation.

The other main kind of, I guess, aspect of my practice which wasn’t something I would have necessarily thought going in is how much of a heart failure doctor I actually am. Dr. Perry knows I am married to a heart failure doctor, Dr. Greg Wood, so sort of an armchair heart failure doctor, but it is really an important aspect of an electrophysiologist’s care, is to recognize the surroundings that these arrhythmias are happening in.

Although it’s true that treating ventricular tachycardias can sometimes make the heart failure better if they are the primary cause, it is also true that when patients are having declines in their heart failure status and maybe needing to move on to more advanced therapies, that they may have more VT. You may be the person who says, “Hey, you do need to start to talk to somebody else about advanced heart failure therapies and what might be prognosis, as well as getting palliative care and goals of care really aligned.” These are serious arrhythmias within the setting of structural heart disease and these can be difficult conversations.

Perry: Perfect. Well, thank you so much for your time. I really appreciate you visiting with me and going over these cases, and I think I learned a lot and had a great discussion.

Robinson: Thank you, Andrew. I think this is a great podcast and thanks for doing it.

Perry: All right. We’ll see you later.

Robinson: Bye.

Andrew Perry, MD, is a cardiology fellow at the University of Washington Medical Center in Seattle.

Last Updated January 15, 2021