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Michelle M. Kittleson, MD, PhD: Welcome to Medscape InDiscussion: Heart Failure. I'm your host, Dr Michelle Kittleson. This is the ninth episode in our 12-part series. Today we're talking about special concerns related to arrhythmias in patients with heart failure. We all know that patients with heart failure are at risk for atrial and ventricular arrhythmias, and patients with arrhythmias are at risk for heart failure. Sometimes the two can coexist, and sometimes optimizing one will fix the other. We're going to focus today on those thorny clinical dilemmas of the interaction between arrhythmias and heart failure. For expert guidance on these questions, we've invited Dr Mark Link, professor of medicine and director of cardiac electrophysiology at The University of Texas Southwestern Medical Center in Dallas, Texas. Welcome, Mark.
Mark S. Link, MD: Michelle, thanks so much for having me.
Kittleson: So, you're a nationally recognized expert in electrophysiology (EP). What was it that sparked your interest? No pun intended. And what keeps you engaged today?
Link: That's an interesting question. I graduated from internal medicine in 1989, and then I went to the Air Force for 4 years. In 1989, EP involved serial EP testing with a subclavian wire, and it was miserable. You hated to get those patients on your service. And what happened in 1990? Ablation came out. In 1992, implantable cardioverter defibrillators (ICDs) were being used, but I didn't know that — I was working with the Air Force. So, when I was interviewing for my cardiology residency, they said, "What do you want to do in cardiology?" And I responded, "Anything but EP. Just don't make me do EP." But it had changed, like Rip Van Winkle. Those 4 years had completely changed EP. When I started my cardiology fellowship, I saw that. I saw that there were ablations. There were devices available and you could fix people, and it was eye opening. I'd always loved arrhythmias, but the practice of EP became exciting, too.
Kittleson: I love that story. I love the serendipity of it. You're in the right place at the right time. An open mind and fertile soil. It's so cool. Let's start with atrial fibrillation (AF) — a clinical conundrum facing heart failure cardiologists that is like the chicken and the egg. Did the AF cause the heart failure? Did the heart failure cause the AF? Do you ever know? And tell us, how does this factor into your decision when you're thinking about rate vs rhythm control for your patients with heart failure and AF?
Link: This is the biggest dilemma we face in the interaction between EP and heart failure. There's no doubt that they coexist. They make each other worse, and you must treat both. Sometimes someone shows up who's in AF at 160 beats a minute but asymptomatic from a palpitations standpoint, and they have an ejection fraction of 20%. Yes, that's probably a tachycardiomyopathy, but usually you don't know. Usually they coexist. In treating them, you must be relatively aggressive for both. Now, when a patient gets admitted with heart failure and they're in AF, the first thing we are asked is to get them back in sinus rhythm. We use a lot of amiodarone, even though the randomized trials would say it doesn't reduce hospitalizations and doesn't reduce mortality. But still we use it because that's kind of all we have for antiarrhythmic drugs. We don't have much else for heart failure, but now what we've got is ablation. Ablation has completely changed the landscape of our ability to deal with AF. Now we can be aggressive with ablation as well, and it offers us more options for treatment. We also can "ablate and pace" — ablate and do cardiac resynchronization therapy (CRT). That's been shown in a randomized study to be beneficial, too. What we've learned is that we do have to be aggressive in our treatment of AF, and that can make the heart failure better. But we have also learned that if you treat heart failure, the risk for AF declines. That's seen especially with CRT. I've had several patients who get CRT who have been in AF for 6 months, and lo and behold, 3 months later, they're in sinus rhythm because their hemodynamics have been improved. So, you must treat both. That's where the heart failure doc and the EP doc must work together, and I think that as a rule, they work together quite well.
Kittleson: I will second that and I will third that. I completely agree. Medicine's a team sport. We're hyperspecialized in our silos, but on the other hand, we still need each other. It sounds like from what you're saying, when you have your patient with heart failure and AF, you treat the two in parallel. My job as a heart failure doc is to get them on the best guideline-directed medical therapy. Then I turn to you and say, "I've done my part to help the AF. You do your part to help the heart failure out by treating the AF."
Now, I have a question for you. When you have a patient who presents with what you presume is a tachycardia-mediated cardiomyopathy, if you just purely rate control them, will that normalize their heart function? Or is there something special in a tachycardia-mediated cardiomyopathy from AF where you can get patients to sinus rhythm? Meaning, is it just the rate that's the problem, or is it the rate plus the rhythm in that situation?
Link: We've learned a lot about that over the last few years. To put it simply, it's the rate and the rhythm. Certainly, the first thing you want to do is slow the heart rate down. Beta-blockers would be ideal. Avoid calcium channel blockers because they depress the heart. So, use beta-blockers first, but this is the kind of patient in whom you would use amiodarone right away, too. You must make sure they don't have a clot, but amiodarone works very well for rate control, and it gives you some time to let their myocardium recover. But what we've also learned is that rate control isn't as good as rhythm control. We'll be reviewing that in some of the trials. That has to do with the regularity of the ventricular response. It has to do with atrial transport of blood. It's better from a sympathetic tone standpoint to have a regular rhythm. There are lots of reasons to think that a regular rhythm would be better than a rate-controlled rhythm at the same rate. It's not always possible, but there are lots of reasons to think that regular atrial contraction is beneficial.
Kittleson: I love the foreshadowing you've provided. Now all of our listeners are on the edges of their seats because they want to hear about CASTLE-AF and CABANA. How have these trials impacted your practice? Why is every electrophysiologist I know so excited about these trials? Tell us about the role of catheter ablation in patients with heart failure and AF.
Link: I would love to, but first, a disclosure. I ablate, so I'm obviously going to be biased toward ablation. The heart failure group doesn't ablate, and it's taken a few years to convince the heart failure group that ablation works. Let's start with CASTLE-AF. This was a groundbreaking trial of around 360 patients. They were randomized, and they all had systolic heart failure and a BIOTRONIK ICD (BIOTRONIK, Inc.; Lake Oswego, Oregon). BIOTRONIK sponsored this trial, so they all had a BIOTRONIK dual-chamber ICD, and you knew exactly how much AF they were having. Half were randomized to ablation and half to the best medical care. What was shown is that in those randomized to ablation, the amount of AF they were having was cut by about two thirds. So, it wasn't eliminated, but it decreased much more than it did in those randomized to medical therapy. What the results showed over time — and the curves start to split around 1-2 years — is that the patients randomized to ablation had an improvement in mortality. The combined endpoint was mortality and hospitalization. Those patients had improvement in that combined endpoint. They also had an improvement in mortality alone. Again, that trial has taken a lot of criticism from the heart failure group.
Let's talk about the CABANA trial now. CABANA was for all-comers. It's not a heart failure trial, but a fair percentage of the participants had heart failure with preserved ejection fraction. Very few of them had heart failure with reduced ejection fraction. Patients were randomized to ablation vs the best medical treatment. What happened with this trial is that of the 1000 patients who were randomized to ablation, 100 didn't get ablation, so all they received was medical therapy. Of the 1000 patients who were randomized to medical therapy, 300 of them got an ablation. So, it's a very messy trial because of the crossovers. If you look at intention to treat and include all the crossovers, the conclusion is that no, it did not reach its endpoint. Although it did have a high bar — mortality is a high bar in AF. We don't generally think AF kills you, but if you take the 900 patients who were given ablation and the 700 who were given medical therapy, it reached statistical significance in mortality and hospitalizations. So, that trial has gotten a lot of criticism, too. Am I a little bit biased about CABANA? Yes, because you can't get benefit if you don't get therapy.
Then, CABANA conducted a substudy of their heart failure patients, and that was in about 700 of the 2000 patients. These patients largely had preserved ejection fraction. What that substudy showed was that those randomized to ablation did better in mortality and heart failure. Now, the reason I think the EP community was more positive about these trials is because they came on the heels of eight or nine other randomized controlled trials in heart failure that all showed a benefit. They didn't all show a benefit in mortality, but they all showed a benefit. They also came on the heels of 20-25 randomized trials comparing ablation with medical therapy. Nearly 95% of these trials showed ablation worked better than medications. So, the results of CASTLE-AF and CABANA come as no surprise to me. Had they been the only two trials out there, I'd say that yes, we need some more trials. But again, they're coming on top of 30-40 randomized trials.
Kittleson: So, when we have a patient with heart failure with reduced ejection fraction who is in chronic AF, asymptomatic, and rate-controlled on guideline-directed medical therapy, should our clinical practice be to involve the electrophysiologist for an expert consultation on whether this patient should be sent for ablation, rather than deferring to the heart failure cardiologist to make the decision on their own?
Link: Not everyone with heart failure and AF should have an ablation, just so I'm clear about that. The patients who shouldn't have an ablation are probably the ones who have been in AF a long time and have a dilated left atrium. We always look at the risk and benefit. The risk in this case is that it's not going to work. Ablation is safe, but why go through it if it's not going to work? We've learned this now, too. Don't wait too long before you ablate patients because it becomes less successful over time. The EAST-AFNET 4 trial has shown that if you wait too long, it's not going to work. Don't send us those patients with an ejection fraction of 10% and a left atrium of 6 cm who've been in AF for 10 years. It's not going to work in those patients. Send us those patients early on in their course when they have paroxysmal AFs or short, persistent AFs. Those are the patients who should get an ablation. I always look at two things when I tell a patient the odds of success: how long they've been in AF and the left atrial size. You look at those two features and decide who should get an ablation. But don't wait too long because as that left atrium dilates, the odds of success are going to be less.
Kittleson: That's so useful — to take your judgment and experience and interpret the results of the clinical trials in that lens because you want to apply therapy to patients who will benefit. That's incredible. Now we'll take a segue away from AF to focus on ventricular arrhythmias and particularly this confusing clinical dilemma of the premature ventricular contraction (PVC)–associated cardiomyopathy. When should we be looking for it? Should patients be routinely screened for it, and when does it reach the threshold when you should consider ablation?
Link: There's been a lot of looking into this, but it's all been retrospective, so there aren't the best data in the world. There appears to be a cut point somewhere between 15% and 20% PVC burden that can cause a cardiomyopathy, and it's causal in those patients because when you ablate the PVCs, the cardiomyopathy gets better. But is 10% enough? Probably not, and certainly under a 10% PVC burden is extremely unlikely to cause a cardiomyopathy. If you see no PVCs on a 12-lead electrocardiogram (EKG), their PVC burden is going to be low. But if you do see PVCs on a 12-lead EKG and the patient has a cardiomyopathy, that's when you should get a 24-hour Holter test to see exactly what their PVC burden is. Not only do you see what their PVC burden is but you also see whether they have monomorphic PVCs or polymorphic PVCs. If they're polymorphic, the odds of success with an ablation are dramatically lower.
Kittleson: I like that tip. If 12 seconds of an EKG are fine, chances are good you're not going to be looking at a PVC burden that's 15% or 20%. But say I do see that the PVC burden with my patient is 15% on my 24-hour ambulatory EKG monitor. I talk to them and say, "I'm so excited! Eureka, there's something here! There's a signal we can go after." And they say, "Ablation? I don't think so. That sounds scary." Is there a role for trying to max out beta-blockers first and reassessing, or are these monomorphic PVCs so intrinsically stubborn that ultimately ablation is the best approach?
Link: We often use beta-blockers, but they don't really suppress the PVCs. They make the symptoms better and they help the cardiomyopathy, but they don't suppress the PVCs. So if a patient is averse to an ablation but you're relatively convinced it's a cardiomyopathy caused by PVCs, this might be someone for whom you now think about using amiodarone. There have been some brave souls who are otherwise healthy and relatively young but have a cardiomyopathy with PVCs who get treated with flecainide and they get better. Again, I'd say that's a brave soul who's braver than me. I wouldn't recommend that. But there have been situations like that, and it's typically for those who have idiopathic right ventricular outflow tract PVCs.
Kittleson: I think we need a footnote here. Kids, do not try this at home without adult supervision. By adult supervision, I mean by an expert in EP, recognizing that Dr Mark Link, an expert, would not endorse this approach. That's always so helpful in medicine, isn't it? Because you have what you think you should do, what the guidelines tell you to do, what the trials tell you to do, and then what the patient feels comfortable doing. It's always great to have a contingency plan. That's a very helpful perspective. Let's now end this whirlwind tour of arrhythmias and heart failure with knowledge gaps and the next big thing. What unanswered clinical questions in EP and heart failure do you hope will be solved in the next 5-10 years?
Link: The big thing is to try to find ways to improve our success with ablation. Again, it's not freedom from any AF but decreasing the burden. Now we have PFA — pulsed field ablation — on the horizon. It's being used in Europe, and it's being studied here in randomized trials. There's a lot of excitement in the EP community about PFA — that it's going to be a more effective way of treating our patients with AF and with less risk. So, I'm very excited about PFA. Anything we can do to help AF and heart failure — again, that's most of what we talked about today because that's the most important thing. Are there ways other than ablation in which we could help with AF? Currently, I'm not aware of any antiarrhythmic drugs being developed by the pharmaceutical companies. I think they've given up on antiarrhythmic drugs, which is probably unfortunate. It'd be great if we had a better drug, although I've always said if we had a drug that prevented AF in everybody, half or two thirds of the electrophysiologists would be out of a job.
Kittleson: We know everyone has mortgages and tuition fees.
Link: The next thing I think is very exciting is this left bundle branch pacing, especially in CRT nonresponders. We need more randomized data — CRT vs left bundle pacing. We've given up on His bundle pacing because the thresholds rise over time, there's a higher dislodging rate, and it's just more difficult to do, whereas left bundle branch pacing is more forgiving. You don't have the typical rise in thresholds, and whereas CRT is dependent on the venous anatomy, a left bundle lead is not dependent on the venous anatomy. There are times when the venous anatomy is so difficult that you can't get the standard left ventricular lead in. So, left bundle pacing is very exciting for us, but what we need to see are randomized trials of left bundle vs traditional coronary sinus leads.
Kittleson: Well, everyone, you heard it here first. We can hope that just as Dr Link emerged from his 4-year Rip Van Winkle slumber and found the miracle of the transformation of EP after medical school, maybe we'll find the same thing over the next few years. Tell us, Dr Link, in closing, what's the one thing you want listeners to do differently after hearing this discussion?
Link: To the heart failure group predominantly, what I would say is send us your patients earlier on with AF. Don't wait till they've had AF for a year or two because the success rates of ablation are going to be lower with that. Send them early, but don't send us all of them. Don't send your patient who's 84 years old who's been in AF for 10 years and has a left atrium of 6 cm. I do not need to see that patient.
Kittleson: I love it. I think the most important thing that's come out of this discussion, like you said, is finding the right patients who will benefit from the right interventions. I'd like to thank you so much for all your wisdom. It's been a pleasure to welcome you here today.
Link: Thanks, Michelle. It's been great. As I tell my kids, I have the best job in the world — even though they won't go into it.
Kittleson: That, my friends, will be a discussion for another podcast. Thank you for joining our discussion with Dr Mark Link. There's much more ahead in the coming episodes, so be sure to check out the Medscape app, and share, save, and subscribe if you enjoyed this episode. I'm Dr Michelle Kittleson for Medscape InDiscussion.
Idiopathic Premature Ventricular Contractions From the Outflow Tract Display an Underlying Substrate That Can Be Unmasked by a Type 2 Brugada Electrocardiographic Pattern at High Right Precordial Leads
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Cite this: Thorny Clinical Dilemmas: Arrhythmias and Heart Failure - Medscape - Aug 08, 2023.