Hi, this is Eric Prostowski and welcome to another segment of EP on EP. With me today is a good friend for years and a real up-and-coming star in our field of electrophysiology, David Frankel, who is the Associate Professor of Medicine at University of Pennsylvania Medical School and the Director of the EP Fellowship. David, welcome to the show. Thank you, Eric. It's truly a pleasure to be here. So today we're going to talk about a subject that is very dear to your heart, no pun intended, pacing-induced cardiomyopathy. We've really researched this area. It's something that I think we really need to know about, and I'm going to take it in three different parts. First, let me ask you, as a clinician, you've put in just a regular RV-based pacemaker and a patient comes back to see you, who are the patients that you worry about, even before doing any tests, that might develop a myopathy? Absolutely. To start with some definitions, we consider pacing-induced cardiomyopathy to occur when the ejection fraction drops by 10% or more, resulting in an ejection fraction of 50% or less. Looking at our experience at Penn and at the published experience at Cleveland Clinic as well, what we found is that the wider your native QRS duration, the more likely you are to go on to develop pacing-induced cardiomyopathy. And this QRS duration is sort of a marker of susceptibility to a variety of different insults. We know that patients with PVCs, the wider the PVC QRS duration, the more likely you are to develop PVC-induced cardiomyopathy. We know that patients with non-ischemic cardiomyopathy and VT, the wider their QRS duration, the more likely they are to die in follow-up or need a heart transplant. So whether it's a marker of diffuse fibrosis, slower cell-to-cell conduction, whatever it is, it really is a pretty robust marker of risk in addition to ejection fraction. And so what we found is if the native QRS duration is more than 115 milliseconds in the absence of a bundle branch block, that's actually highly specific that the patient will go on to develop pacing-induced cardiomyopathy. The other marker of risk that we found, interestingly, was being a man. We know that there are some gender differences in susceptibility to various cardiomyopathies, myocarditis, stress-induced myocarditis, et cetera. We found the same with pacing-induced cardiomyopathy. So I remember that paper, viewers, the specificity I remember, but what is the sensitivity of the native QRS, David? Yeah. We chose that marker to be very specific with the idea that this is a patient you might want to think about biventricular pacing up front or conduction system pacing up front. So if the QRS duration was more than 115 milliseconds, again, not a right bundle branch block or left bundle branch block, then that patient was 90% likely to go on to develop pacing-induced cardiomyopathy. So very specific. Most patients who go on to develop pacing-induced cardiomyopathy are not that wide at the beginning. So it's not sensitive. And then two other issues to think about, which are important. One is pacing burden. I think that there's this number that people have in their mind of 40%, which comes from the MOST trial. And what MOST showed was that if you RV paced 40%, you were five times as likely to be hospitalized for heart failure as patients who didn't RV pace. But even in MOST, if you were pacing 20%, you were still two to three times more likely to be hospitalized for heart failure as someone not pacing at all. So actually, in our experience, as well as Cleveland Clinic, 20% RV pacing is enough to develop pacing-induced cardiomyopathy. And of course, that's analogous to PVC-induced cardiomyopathy, for example, where a PVC burden as low as 12%, maybe even 10%, can cause a cardiomyopathy. So that number of 40% is not exactly right. We need to start thinking about this when your patient is exposed to 20% or more pacing. So we've got two of the legs of this three-legged stool, because I know there's another one that you've also done research on, and then I want to put it all together for our listeners. So then you have the predisposing QRS, then you have the duration of V pacing, but then you also have, if I remember, another paper of yours, the duration of the QRS paced. Maybe you can talk about that. Yeah, absolutely. And that gets to the next question. You said there's three items on our agenda today. So we talked about who do you need to worry about developing pacing-induced cardiomyopathy? And the next question gets to follow-up, paced QRS duration, and who do you need to worry has now developed pacing-induced cardiomyopathy? And so the first thing that I think we all know, you can't wait for patients to develop heart failure symptoms. Their EF easily could drop 10% to 15% without clinical manifestations. So only half of patients in our series who had pacing-induced cardiomyopathy presented with symptoms at the time of that first diagnostic echo. So it's better to take an active surveillance strategy where you're looking for this. One thing we found is that that paced QRS duration, if it's less than 150 milliseconds, it's almost unheard of to have pacing-induced cardiomyopathy. So this is, as opposed to the 115 on the native QRS duration, which is highly specific, 150 on the paced is highly sensitive. So almost anyone who has pacing-induced cardiomyopathy, their paced QRS duration is going to be 150 or wider. So I think a reasonable approach would be once your patient's paced QRS duration gets to 150 milliseconds, then start doing those surveillance echoes every one to two years to look for an actual decrease in ejection fraction. All right. So let me put this together then, the way I look at it for me. I've used actually some of your research, David, to help me as I look forward, as I follow my own patients, because like you said, you don't want the person coming in with an EF of 25% when you could have aborted the process, right? So I totally agree with you there. I've been using that myself, but you've been looking at this so long, I don't have an algorithm of all three. So, I mean, I don't, I'll be honest with you, I've probably forgotten by the time I see the patient back a year later what their original QRS duration was. And I probably ought to note it somewhere in the EMR, but I certainly look at how much they're pacing in the duration of the QRS paced. And I kind of use what you've said, if they're doing at least 25 to 30% pacing and the QRS duration is above 150, I'll usually get an echo. Is that sort of what you're saying? Yes, that's exactly right, Eric. So when a patient is pacing 20% or more and the paced QRS duration is 150 milliseconds or wider, that's the time to start doing your screening echocardiograms every one to two years. Okay. I was going to ask you, every one to two years, I'm never sure how often to do it. Sometimes you lose the patient for a while, then they come back and it's been three years. And as you said, the vast majority of these people, if you've done it right, do not have symptoms. So you're trying to catch them early. So I think every year, at least for me, David, is maybe too much. I like the two-year mark, but I guess I could miss someone. Yeah, I think two years is very reasonable. And moving into stage three of the conversation here, the beauty of pacing-induced cardiomyopathy is that it is very reversible when you upgrade to CRT. And that's why I think a two-year screening window is absolutely appropriate, because I think the window to upgrade to CRT and to resolve that cardiomyopathy seems to remain open for a long time. So our experience is that patients with a pure pacing-induced cardiomyopathy do extremely well following CRT upgrade. And so let me explain what I mean. Well, let me interrupt you only for a moment, because I know, because we've discussed this before, you've actually leapfrogged something that I know you do in between. And I want to make sure the listening audience understands it. I know you don't just assume that it's a myopathy, but you do look for other things so you don't miss something, correct? That's extremely important. So really, it's a diagnosis of exclusion. You want to rule out the common things, coronary artery disease, uncontrolled atrial fibrillation, frequent PVCs, uncontrolled hypertension, severe valvular heart disease, and even thinking more specifically about the context of complete heart block, sarcoidosis, Lamin cardiomyopathy, you know, that is not pacing-induced cardiomyopathy. Pacing-induced cardiomyopathy is what you're left with when the ejection fraction drops and you've ruled out all that other stuff. Yeah, right. I just wanted to make sure you brought it out, because I know that's what you do. So let's assume now you've done that, now you're on to, what do you do next? What do you do next? So the short answer is upgrade to a CRT pacemaker. And the reason is, is that patients do really well. So in our experience, about 80% of patients will improve by at least 10% in their ejection fraction. And even patients with what we call severe pacing-induced cardiomyopathy, meaning bringing their EF below 35, the vast majority of those are going to improve and clear above 35% with the CRT. So it seems to be a very reversible cardiomyopathy. Cleveland Clinic described a similar high response rate as well. So you know, if it's a patient you think has pure pacing-induced cardiomyopathy, I think just adding a simple LD lead and making it a biventricular pacemaker is great. Of course, you were driving at this point before, and it's extremely important. If your patient's EF has gone from normal to 30% in the setting of RVD pacing, and they have cardiac sarcoidosis, totally different ballgame. That patient's not going to get, it's not going to normalize with CRT. So that patient needs a biventricular defibrillator. But when you think it's pure pacing-induced cardiomyopathy, I think starting with a simple procedure, upgrading to a biventricular pacemaker is an appropriate start. So let me challenge you on just one thing, because I really buy everything, except I'm a little maybe more conservative. Patient today came back and saw me, ironically, this was perfect segue for today's show. I mean, I didn't know he was coming back. But he had a EF that went from about 55 to 60. Our echo readers tend to give us a range, so down to 40 to 45. And I, over the period of about two and a half months, gave him some carbadolol and a little enalapril, and then repeated the EF, and it was back up to 50 to 55. So I did not upgrade him. I actually don't think there's any problem with that, and I wanted to get your views on that. I agree 100%, and thanks for bringing that up. Heart failure medications are extremely important, and whether you are upgrading to CRT or not, the patient should be on a beta blocker and an ACE inhibitor, because we know those work in all cardiomyopathies. And you may save your patient a procedure. You may help them improve in conjunction with the CRT. So it's not one or the other, it's both. And taking the clinical context into consideration when you're deciding whether to do the upgrade is obviously very important, as well. Is it a younger patient? You may tend to be more aggressive, because they're looking at decades and decades of RV pacing. Is it an older patient whose EF is 45, but they're feeling absolutely fine, and their quality of life is unaffected? Well, that's not someone there's any rush to do another procedure on. So I think you're absolutely correct. So David, this has been an incredibly useful, clinically useful session. I'm going to summarize it and see if I mess up or not. As I get older, I may mess up a little more than I used to. So the three-legged stool to begin with is look at the narrow, look at the QRS to start with, look at how much pacing you are in the QRS pace duration. Second section of your interview is once you've figured that out that there's been a fall, I think you said at least 10% of the ejection fraction, if I remember correctly, then look for other causes, seeing none, move on to good medical therapy, as well as an upgrade to a CRTP. Do I have it? You got it. You nailed it. It's good. I'm glad you didn't ask me to be an hour from now. Listen, David, it's been great. Thank you so much for being a guest and imparting your knowledge on this important topic. Thank you so much for having me, Eric. It's been fun. Thank you.

pacing-induced cardiomyopathy

QRS duration

male

echocardiograms

cardiac resynchronization therapy (CRT)