Hi, this is Eric Kostowski and welcome to another segment of EP on EP. This is really a very timely segment and we've got really one of the experts in the country in this area. Dr. Janet Han is joining us and she's the associate professor of medicine at UCLA in the Cardiac Arrhythmia Center. She's going to discuss with us arrhythmias and COVID-19. So Janet, welcome. Thank you. It's lovely to be here with you today. Now, I'm going to start kind of like the Bible in Genesis, in the beginning, because it was crazy, right? I mean, we were all like faced with something we've never been faced with before. It was helter-skelter, and I know you were in the thick of it, so why don't you start off this segment by telling us kind of what it was like when you were first faced, especially in your center, with what was going on from like what the theories were, what the initial thoughts were, and maybe even therapies, and then we'll move on to kind of the later stage. So I think you hit it on the nose when you said that things were helter-skelter because I think there's a sort of weird sort of frantic feeling that I think we all had, and I know that we were on a lot of calls together through HRS, and we got together with our colleagues from across the nation, across the world, and we were all kind of seeing different things kind of depending on where we were. I know that New York got very hard hit at the very beginning, and I remember talking to my colleagues there and then starting to see some of that stuff out here in the West, but what was funny is we kind of were seeing a smattering of all kinds of arrhythmias at the beginning because, again, there was sort of this frantic trying to keep very, very sick people alive and trying to understand this disease process. So I know in my institution, we started to see a lot more sort of the Brady arrhythmias, which was interesting, and we can kind of get into that a little bit later, and I remember sort of getting geared up in all of, you know, all the PPE and implanting a bunch of pacemakers sort of at the very, very beginning, and I remember talking to friends in New York who were kind of seeing similarly things like severe bradycardia and PEA and people sort of dying on the spot from sort of being normal sinus rhythm, sinus tach, and then suddenly PEA and dying, and then we were hearing all kinds of other things out of China, too, about how people would have, you know, up to 16% arrhythmias, some of which were ventricular tachycardia, and we were all, you know, got very nervous about maybe people were going to have myocarditis and fulminant, you know, cardiac failure and lots of VT storm, which, you know, we ended up, you know, not seeing a lot of that here either, you know, out west or in the East Coast. So I feel like at the very beginning, it was mad. It was just absolutely madness, just kind of trying to find our feet a little bit about arrhythmias, and then I think after that, things kind of, I don't want to say settled down, but there was sort of a lull after the first peak that we kind of caught our breath, so to speak, a little bit, and then we were able to sit back a little bit and really look at our patients, and a lot more studies came out at that time, once we had that sort of breather, to take a good look sort of retrospectively at the patient population and what we were seeing. And that's great as a start. Let's talk just very briefly, because I don't know it deserves another talk, but remember all that QT madness. I mean, it was driving me nuts, and, you know, the therapies, that sort of faded into the distance, right? It never really materialized. Yeah, I think, you know, we, I think, you know, we were on so many calls about that, as you know, and I think we were really scared about that because of how so much hydroxychloroquine and azithromycin was being used, and I think we were very nervous that people were just going to bump out their QTs and have a lot of TORSAD, really, on top of what we thought was, again, going to be this fulminant myocarditis and VT storm, so I think that's sort of what spurred us to sort of give this guidance a little bit, and, you know, everyone was coming up with all of these algorithms of how to, like, measure the QT and how often, and, you know, make sure you're not on all the other QT prolonging drugs and check the lights and all this kind of stuff, right, but what's interesting is that we ended up not really seeing a lot of that after, you know, now we're like 400 and something odd days into this. We haven't really seen a lot of QT prolongation now. I gotta tell you, you know, after I gave that other talk with you at your other symposium, the New York group put out another paper about QT prolongation in COVID patients, and they did end up, you know, looking retrospectively. They did look at about 3,000 or so patients, and they did find that COVID-positive patients tended to bump their QT out by about 20 or, you know, 20 to 30 milliseconds more so than non-COVID patients did, but, you know, they only had one patient with TORSAD, so that's a, you know, tiny proportion, really. Yeah. And if you remember my irreverent comment on our committee, I said there are more algorithms that take care of prolonged QT than prolonged QT patients. Right. Yeah. That's a problem, right? Yeah. That is a problem. Right. Indeed. So let's move, then, to the data accumulation phase. Yeah. You get through that initial thing. You and others were collecting hard-core data. What did we learn at that point, then, about what a rhythm is legitimately we're seeing more frequently? Issues about sudden death. Can you get into that a little bit? Yeah. Sure. So really what we ended up understanding is, so we ended up sending out our own survey at the very beginning of the pandemic, and we got back about 1,200 responses, and that was sort of the first sort of measurement of what we probably were going to be seeing, and it was interesting because once we looked at that and then now look back on that study, it was pretty much predictive of what we're seeing now, which is we found that probably about a third were atrial arrhythmias, about a quarter was bradyarrhythmias, and about 10% were ventricular arrhythmias, and then as things, again, settled, as the dust sort of settled, we found it was even less than that, right? So the biggest player that we found now is that it's really atrial arrhythmias and AFib, probably the biggest thing, and when you really shake down the data even more, like if you look at the Get With Guidelines COVID registry or the AHA registry, they found that really AFib was about 8% out of all this. So we thought a third, other institutions, as they were starting to write their papers sort of towards the middle of the pandemic, were seeing about 10% to sort of 20% AFib, and so it settled down to being about that 8% to 10% range again for atrial fibrillation. VT-wise, very little, definitely less than 10%, more along the lines of 5% or so, and then bradyarrhythmias, again, only smatterings of case reports, so really very, very low, so tiny, tiny bits of bradyarrhythmias, and so I think the last thing I'll say about AFib is we sort of have to sort of talk about mechanism a little bit because I know that other people have sort of asked, well, isn't it just that people are sick and they're going to get AFib, right? So Vivek Reddy's group just published a paper in Jack EP that they compared the COVID patients to flu patients, and they found really it was about the same. So they found about this 10-ish percent of AFib in both sets of patients, and the new onset AFib was really about 4%, and so they said, you know, it's probably just from acute illness that these people are getting AFib. So let's stay with that a little bit. I had a couple patients, and they did not have COVID. For me, the emotional stress of the time in the March, April, May part, I had two people who we ablated probably 10 years ago, and they both came down with AFib. One was six years. One was 10 years. They didn't have COVID. They were sheltered at home, but they were emotionally so distraught that they both had a recurrence of AFib for the first time and then no longer had AFib. I mean, it lasted a couple days, and it went away. So I suspect there was some emotional overlay. Is that something you also experienced? Yeah, that's interesting because I don't think there's any studies that really have looked at that. The studies that are out there really are looking at in-hospital super sick COVID patients more than anything else as far as the AFib goes. So a lot of this data comes from the ICU population, so you're going to see a lot more AFib, obviously, in that very sick population. There was one that I remember, a study that looked at an outpatient population, and even in that study, they hardly saw any arrhythmias, period. And it was like 700 patients, I think it was from Penn, and I think they saw a total of nine patients or something with AFib. So it's still a tiny proportion of any arrhythmias when you're not super sick with COVID. So I think you're right. Oh, I'm sorry. I interrupted you. Finish your statement. No, I was going to say, I think you're right. I think there probably is going to be some emotional component to some of it because you do see it. I think some people have said, oh, I've seen some patients get the vaccine and they get AFib, right? So I don't know if people are a little nervous or sympathetically charged. Yeah. I agree with you there. I'm not going to even discuss vaccine. No. I'm not going there. It's such a hot topic. Right. But let's go to now, to the present, right? And that's a fantastic journey to this point. Two things that I wanted you to address. Number one, the AFib that was seen, I don't know, because we didn't put a series together like you guys did. Is that acute AFib and it's not come back? That's the first question I have for you. And the second is, we're trying to deal with these reports of myocarditis and then we'll get, last of all, into the autonomic dysfunction. And the reason I bring up the myocarditis bit, I've been looking for that. I haven't found one yet of a positive delayed enhancement. Yeah, we saw those early reports. So update us on those issues, please. Yeah. So I think, as far as, I'll take the myocarditis one first. So myocarditis is interesting because I think people are so nervous about that, right? Because at the very beginning, it was this whole fulminant cardiac failure, myocarditis, horrible badness, right? And then there was a tiny study, 40 or so patients, 30 or 40 patients about the athletes, right, that were having myocarditis. And that really set people off. And I think they found some like 40% LGE or something horrible. And so then all the athletes got sidelined. But then when really people looked at it, and then I think our institution was also involved, and I think Duke was involved, maybe Stanford as well. And they did this 800 patient athlete study comparing them with athletes. And what they found really is the myocarditis incidence, bottom line, was less than a percent. It was like 0.3. So you have to remember, athletes have LGE because of their overtraining, right? Or their, you know, large amount of training. So they have LGE in certain parts of their heart that could be misinterpreted as myocarditis if you compare them to like a normal non-athletic population. But if you compare athletes to athletes, the true incidence of myocarditis from COVID is tiny. It's like less than a percent. So am I over-testing them? Because I was not actively taking care of COVID patients at our institution. But I've seen a whole bunch of people who've had COVID come back. And, you know, they have a variety of things. Not necessarily that much different than they had before. I've done several CMEs, you know. I mean, you know, CMRs, and I've looked for myocarditis. I'm thinking maybe I'm over-testing people. I mean, I don't know. Is there an indication to do, you know, to get a cardiac MRI to be sure? What are your thoughts? Yeah, I think, you know, I kind of take it the way that that paper, the biggest paper about athletes takes it, which is you should have other signs or symptoms of cardiac involvement before you jump to the MR. I think that's probably the best way to say it. You know, do your EKG, do your echo, and if those are abnormal, then jump to the MR. So I'm going to end our clinical discussion with a problem that we all do not want to see. And we feel very bad for these people, but it's out there, right? And that's these autonomic dysfunctions. I mean, I've learned a lot about POTS. I've had one of those patients, but I've had actually more infiltrated sinus tachypathy patients come, who probably had the problem before, but it's magnified. What do you have to offer us on that as far as, is there anything different you do for them? What do you tell them? Yeah, I think we, first thing I'd have to say is with this sort of long COVID, I think we have to be very, very careful about what we say at all about long COVID, because I just don't think we understand enough about it. Just like, you know, I liken it to the beginning of COVID, where we just didn't understand it. And so we're kind of throwing lots of things out there. I think long COVID, I think we have to be very, very careful about what associations we make. Now, that being said, I think we do understand that there probably is some autonomic dysfunction type symptoms that have come up with long COVID, including stuff that acts sort of POTS-like, right? So sinus attack, like you were saying, a little hypotension in some people, or orthostatic intolerance, I should call it. And just like other vague symptoms, you know, like sleep disturbance and headache and that sort of stuff. And then when you put them on tilt, they sure act like POTS. And so people have been treating them like POTS, you know, with like fluids and sort of, you know, those sorts of things. And then secondarily starting them on meds if they need to be on meds. But really it's more like orthostatic training and conservative management until we sort of figure out what to do. Because, again, we don't know exactly what it is and we don't know exactly what to do yet. But treating it conservatively is probably reasonable. I have had a couple patients who came in with rates of POTS. I mean, they weren't POTS, they were ISP. And I will say they responded very nicely to our liberty. So I'm suspecting you're finding the same thing. What I don't know is if they always sort of had it and now it's become more manifest because they went through. I'm having a hard time figuring that out. I don't know what your experience has been with that. Yeah, I think we don't know. Again, you know, there still has to be time, right? Because, again, it's like we just finished a year of horrible pandemic and now we're seeing the fallout and we've only seen the fallout for probably three to six months, something like that. So I think we need more time. Well, I want to tell you it's been a great discussion. And I want to personally thank you. I remember those first few months we were on the HRS panel together. I was not doing my work. I wanted to congratulate you and your colleagues who were putting on the PPEs and getting in those rooms and helping us try to understand that you deserve our gratitude. And so thank you for all the hard work you did. And thank you for the update. And I appreciate you joining the show. Thank you so much. I had a great time. Thank you.

arrhythmias

COVID-19

AFib

myocarditis

autonomic dysfunctions