It's a debate that's been running for a long time. We're going to try to keep things close to target. My co-moderator, I'm John Fisher, and my co-moderator is Dr. Kim. We are fortunate to have here Dr. Megan Labreck and Dr. John Hummel, both from Ohio, or the state of Ohio. So that ought to increase the excitement as they spar back and forth. We're going to try to keep closely to time. So the first speaker will be Dr. Labreck, who will be talking to us about loading type 1c or type 3 antiarrhythmic drugs. Is it OK to do that as an outpatient or inpatient or both or neither? And she's going to let us know her views on that. Thank you. Thank you for that kind introduction. All right, so we'll go ahead and get started. So we're going to discuss outpatient versus inpatient drug loading. So pro-outpatient drug loading and the importance of keeping bed space open in our ever-growing population of AFib patients that are taking up bed spaces in our hospital systems. Also, the increased reimbursement of outpatient procedures versus inpatient procedures and our overall patient satisfaction. So in regards to our oral antiarrhythmic drugs that we can consider initiating in the outpatient setting, in regards to the class 1c drugs, so flecainide and propafinone, we all know from the CAST trial, of course, that the absence of structural heart disease in a normal EF, if we're looking at these patients to start an antiarrhythmic drug, if we're starting propafinone or flecainide, it's important to take an accurate and complete history, make sure that they have a normal echo that is recent, and then appropriately assess for a stress test or order one if it has not been done prior to starting that therapy. And it's imperative that a patient take an avianodal blocker with those agents, given the risk of one-to-one flutter and possibly the progression to wide complex tachycardia. So we can initiate these safely in the outpatient setting if patients have close follow-up. And those boxes is checked for no structural abnormalities or reduced EF. In regards to class 3 drugs, unfortunately, with the risk of torsades and ticosin, it's still recommended that we do that inpatient with close monitoring. But Sotilol, however, has been a rather controversial topic. So outpatient initiation, I think, goes on more than it may be documented. But Sotilol initiation would be safe and recommended outpatient in patients with either atrial or ventricular arrhythmias. If patients don't have a history of torsades, have normal renal function that is either notably stable or has minimal ability to it, normal QT at baseline. If they have an implant, maybe their renal function is a little labile, but they do have that backup. And patients that are willing to undergo monitoring, whether that's routine 12 leads or mobile ECG follow-up or some other wearable device, it would give us a relatively accurate measurement of the QT. Some real-world data that we have in regards to outpatient Sotilol initiation. So Dr. Sanders' team down in Adelaide, Australia, published a paper that had about 888 patients that they followed over the course of 2008 to 2023 that was published last year, just prior to HRS, that demonstrated a very rare QT prolongation. And 95% of patients underwent successful initiation and maintenance dosing. The patients that did not continue on Sotilol were patients that had some bradycardia that required dose adjustment. There was no Sotilol-related mortality or ventricular arrhythmia or torsades, notably. And they performed ECG monitoring at day three, seven, and one month. The cohort at Ohio Health that was published in JACK in August of last year followed 263 patients over the course of about just under three years, noted no QT, C prolongation, or episodes of ventricular arrhythmias. And monitoring was done via the same process that would be done for TQS inpatient or Sotilol inpatient, six doses, two hours post-dose, with a cardiomobile ECG. So twice a day monitoring with that. And then Dr. Mascherina's cohort that was published with following four years of 105 patients with implantable device. Sotilol was initiated at 40 milligrams twice a day or 80 milligrams twice a day. So low doses, but had no episodes of torsades or any clinically relevant QTC prolongation. Discontinuation rate was rather high at 27%, mostly due to inefficacy, so recurrent arrhythmia, or bradycardia and perceived side effects, like dizziness, that patients couldn't tolerate. So overall, the risk of torsades has been reported very, very low. The risk of proarrhythmia, very low. So outpatient initiation seems like a really great option, especially if it's convenient for the patient. Having early rhythm control, what we know from eSAFNet is important. So as patients are diagnosed earlier downstream, what is that going to look like? Are they going to have more drug changes down the line? With our minimal options for treatment in antiarrhythmic drugs, it is important that we keep these options open for patients and minimize time spent inpatient. So since we have improvements in diagnostic and screening tools and monitoring tools, we can utilize this to our benefit. So keeping bed space open for more acute patients, keeping those spaces open for our post-procedure patients that may need them. An outpatient reimbursement of procedures is higher versus a bundled hospital reimbursement. So should your patients require cardioversion post-initiation of Sotilol in the outpatient, or even post-conversion, if they don't convert on a 1C? Ordering that as an outpatient procedure leads to higher reimbursement for your institution. So I will allow Dr. Hummel to try to convince us that we should all do this inpatient in his maize and blue tie. Thank you, Dr. Labreck. Let me see here. How do I get to my slides? Let's see. I think this is it. OK. Here we go. So my name's John Hummel. I'm from The Ohio State University. Dr. Labreck gave me grief for my maize and blue tie, which I think is reasonable. I'm here to defend the proposition that anerythmic medications, 1C and 3, should be initiated in the hospital. Nothing to disclose relating to this discussion. I will give an initial concession, and that is that my wife says, don't should people. So I would say anerythmics would best be initiated in the hospital. Or some anerythmics should be initiated in the hospital. Or they're most safely initiated in the hospital. But I'll end this slide with a comment that really is my conclusion. And that is that for most practice situations in the US, anerythmic medications, 1C and 3, should be initiated in the hospital. Now, how to make such a decision? There are some landmarks over the past 20 to 30 years that point the way. FDA black box warnings are the strongest warning the FDA requires that drugs carry a significant risk of preventable, serious, and even life-threatening adverse events. And then there are our professional society guidelines that define practices meeting the needs of the patients in most, but not all, circumstances. And they don't replace clinical judgment. So what do the black box labeling of sotalol, defedolide, et cetera, tell us? Well, sotalol and defedolide, quote, should be initiated or reinitiated in a facility that can provide cardiac resuscitation and continuous electrocardiographic monitoring. Interestingly, preparing for this, amiodarone still carries that same labeling. But propafenone, flecainide, donaderone have no black box labeling regarding initiation. The guidelines actually diverge a great deal from this. Defedolide and sotalol confer a relatively high risk of torsades. Patients need to be admitted and closely monitored when starting or reinitiating defedolide, as well as for increase in the dosage. But when it comes to sotalol, as Dr. Labreck implied, there is a little more controversy. They say it softens dramatically. Many practitioners choose to initiate sotalol in an inpatient setting, that's what they say. And then amiodarone, flecainide, and propafenol can be started in the outpatient setting except when you're using pill in the pocket, may be performed in a monitored environment if a high dose is used, is pill in the pocket used any other way? So they're recommending monitoring that. So what do we know about outpatient sotalol loadering? Well, Dr. Labreck just went through this and her published manuscript of 263 patients using the cardiomobile for a six lead for QTC monitoring is really a tour de force. But to those of you that are thinking about starting sotalol as an outpatient, keep in mind that in this protocol, patients could be in a fibrosinus, they had to meet QTC cutoffs, creatinines had to be greater than or equal to 30, optimize MAG and K, prior EP evaluation, they had to own a cell phone and have no dexterity issues or have assistance at home, access to an online patient portal and know how to use it, they had an EF of greater than or equal to 45%, no syncope, no sustained VT without ICD, no QT prolonging drugs, no recent acute MI, dedicated pharmacist aneurysmic clinic, cardio training, sotalol training, and the protocol required an initial visit and then a three patient day outpatient loading with daily examination of the cardiomobile QT with a message from the pharmacist as to whether to continue the drug or not. And then after that, a one week follow up in person. That's a lot. All right, can you do this? I mean, granted, the outcomes were perfect. 95% adherence to the cardiomobile, no patients discontinued the drug, but wow, okay. Maceranus, Brock Cantheria's group, they looked at both dofetilide and sotalol, but keep in mind what was briefly mentioned and that is the doses were 40 BID or 80 BID, okay. And in two different trials, no difference between those low dose sotalol and beta blockade in aneurysmic effect. EF's greater than 55%. They had to be able to transmit their implantable device data. And they had to do this daily and were seen daily and then at one week, two weeks, one month and every three months. When you look at the group from Adelaide that she talked about, again, low dose sotalol, less prescriptive, EKGs at baseline, day three, day seven, one month with very little events, but implantable devices as well. So it looks like we can do sotalol as an outpatient, but just as it begins to look that way, the guidelines downgraded sotalol use. It's third tier when you're looking at normal hearts and structurally abnormal hearts, it's second tier. Why would they do such an awful thing? Well, if you look at the Cochrane database, sotalol use in LVH, CHF, QTCs greater than 150 or bradycardia is associated with torsades and increased mortality. SAFIRE-D study did reasonably well. VF events were less than 1%, but a retrospective cohort of 378 patients looking at dofetilide and sotalol showed no difference in the incidence of torsades at around 1.3 to 1.2%. Diamond AF showed 1.6%. The SAFETI trial that did outpatient loads of amiodarone, sotalol, placebo showed 15 deaths occurred in the sotalol group, eight of which were sudden. There was a retrospective cohort study of 120 patients undergoing inpatient sotalol initiation. Two of the seven VT events were torsades and 20 of the patients had to have their drug stopped, did bradyarrhythmias, we already went over Cochrane. And then the retrospective study of 329 patients looked at dofetilide or sotalol and 76% of the adverse events were QTC prolongation or ventricular arrhythmias. And importantly, in sotalol patients, there were no predictors, whereas in dofetilide, you could predict that based on the QTC. Well, that's exhausting. So what do we do? Well, there is now IV sotalol and it looks like we'll soon have IV dofetilide. The FDA approved IV sotalol followed by two oral doses in the hospital. The peaks registry showed that you can do this very safely. Only eight patients had to stop the drug and the mean length of stay was 1.1 days. So 95% of them were discharged within one night. DASH-AF said, we're not gonna give them two doses, we're just gonna give them IV and then one oral dose and get them out the door the same day. But those patients wore mobile cardiac telemetries and they followed the QT intervals after they left. Now, only four of them had dose reductions. But again, it requires more work and maintenance. So in my view, the problems with sotalol and dofetilide outpatient loading is that there's a lack of predictable effect on individual repol. There's a need for absolute compliance with the EKG and remote downloads. There can be tech challenges in older patients and how compliant are your patients? Maybe they're different than mine. A lack of resources to monitor patients remotely can be a real issue. And most importantly, you have to have a pharmacist or an RN like Dr. Labreck who can follow these patients and have specialized knowledge about drug-drug interactions and is compulsive about it. Furthermore, there's a lack of accurate medication profiles. 40% of our EMR profile, medication profiles are actually accurate. And the IV alternatives for sotalol allows a nearly outpatient load without having to do all this dramatic work. What about the other drugs? FDA black box labeling for amiodarone's a little bit onerous but the guidelines give you a lot of relief. We started as an outpatient, most people do, and the other drugs can be started as outpatients but there's this worry about pill in the pocket. I think in our center, amiodarone is only initiated inpatient for high dose amiodarone or IV loading to achieve early rhythm of rate control and to assess for bradyarrhythmias in patients that we're concerned about. And keep in mind with dronetarone, it's only approved for patients in normal sinus rhythm with PAF or persistent AF and they have a black box labeling that these patients be monitored every three months. Pill in the pocket for 1Cs, this is right out of the guidelines, the AF conversion rates are great, 58 to 68% for flaconide, better than propafenone, but the incidence of adverse effects requiring intervention was anywhere from six to 17% and in the guidelines they say the pill in the pocket strategy should only be used for highly selected patients and after it has first been observed to be safe and effective in the inpatient setting. There were two studies where there was initiation in the emergency department and showed exactly the same numbers, basically, 5 to 16% having side effects requiring acute intervention. The European studies of IV propofenone and IV flecainide load showed you could not predict with the IV loads who was going to have an adverse effect with pill-in-the-pocket high dose. Outpatient 1C initiation at normal doses looks very reasonable based on the meta-analysis and structured normal hearts. The French AF trial demonstrated safety of outpatient initiation. I'm going to put a plug in for exercise testing. QRS widening greater than 25% is predictive of ventricular proarrhythmia in the 1Cs. We did a study at Ohio State looking at 300 atrial arrhythmia patients who underwent treadmill testing after their inpatient load of their 1C agent. Seven percent stopped the drug due to proarrhythmia or ischemia and the treadmill was the only variable affecting decision to discontinue the drug with multivariate logistic regression analysis. There was also a case report, interestingly, of a type 1 brugada that was brought out in a patient on flecainide. So you can also even make the diagnosis of brugada. Guidelines in terms of treadmill do not recommend it. They did in 2014, but it's not included in the current guidelines. So in conclusion, I think the data support outpatient initiation of certain class 3 and 1C anarrhythmic drugs in select patients in centers that are equipped to screen the patients appropriately, provide education and counseling, provide daily, weekly, quarterly reassessment of safety and efficacy. Inpatient initiation of defedolide and the initial pill in the pocket 1C appears to be the standard of care and shared decision making regarding an outpatient initiation should be thoroughly discussed with the patient and documented in the chart. There are medical legal ramifications of bad outcomes. Thank you. Thank you very much. So we'd like to have the rebutter from the Dr. Megan Rubrik for five minutes. That was very thorough, Dr. Hummel. Well, I do agree that documentation and patient selection is very important for outpatient initiation. I think it's also important to consider the cost savings and having a dedicated provider or service for this can be achieved at your institution with the cost savings analysis that has previously been published on this very topic. So inpatient initiation, and this is going to be a little bit So inpatient initiation, and this is cost analysis done back in 2022, so a little bit dated and probably a little bit higher, costs the patient just above $7,500. As an outpatient, in regards to medication costs and the charge of the visit and the EKG, outpatient initiation in total costs just under $900. So significant cost savings, especially in a large throughput center such as either of ours, which does, you know, upwards of, you know, 100, 150 loads every six months, I would say. So again, this is good for patients, good for physicians, good for the health system. Important for the pharmacist to start fostering or dedicated provider to start fostering the relationship among the care team. HRS is endorsing a multidisciplinary care team for the management of our complex AF patients and ultimately protecting the patient safety in this multidisciplinary matter in regards to, like you mentioned, the legal risk to the hospital and the practitioner. Like reported in the data, there is a very low incidence of Torsades in regards to Sotilol patients. Again, this may be due to the low dosing that was originally prescribed. However, in a dedicated clinic that may be able to optimize these patients, using the cost savings measures, having patients with increased access to wearables, the increased utilization of these despite age and socioeconomic class, patient preference for outpatient monitoring. We can have patients decrease the time they have to be away from family and time away from work. And we can have patients safely monitored on these with mitigation measures. We can have patients safely monitored on these with meticulous follow-up. And interestingly enough, published about two weeks ago, Marino and colleagues in ERA and ESC published their compendium on antiarrhythmic drugs, which recommends inpatient or supports, I should say, inpatient versus outpatient initiation of the following drugs, which notes that outpatient can be considered inpatients that meet certain criteria, which would be stable patients without structural heart disease and no evidence of previous proarrhythmia from other antiarrhythmic drugs. So with that, I leave you with the support of outpatient initiation of certain antiarrhythmic drugs if patients meet criteria for such and are not at risk for proarrhythmia. Thank you. Thank you. There we go. Thank you. So a couple of interesting surveys. Two large surveys show that physicians that initiate these medications believe the guidelines for antiarrhythmic medications should be followed. It's like almost 98%. But when you look at their behavior, they often don't follow them in terms of the characteristics of the patients receiving medications. I mean, if we look here at the Class 1Cs, 6% to 18% are given in patients with coronary disease, heart failure with reduced EF, HEF-PEF. And you look over here at dofetilide, 18% or 16% are initiated as outpatients. Amiodarone is given first line for patients with structured normal hearts. So we don't really do what we say. If you look at dofetilide, a survey said that the guidelines should be followed and found that 67% initiate dofetilide as an inpatient. The rest initiate it as an outpatient. And then 78% reinitiate the drug as an outpatient, which is completely off guidelines. So I think one of the advantages to in-hospital loading is that it saves us from ourselves. This allows input from the pharmacist, the APPs, and colleagues on the inappropriateness of what you're doing for the inpatient and drug-drug incompatibilities. It allows direct observation of the effect of the anerythmic on the arrhythmia and surveillance for bradyarrhythmias, atrial proarrhythmia with conversion to flutter with a rapid ventricular response, the ventricular proarrhythmias, negative inotropic effects, and drug intolerance. And it limits medical-legal exposure and allows rapid treatment of anerythmic-induced proarrhythmias. I would say that at the end of the day, outpatient initiation versus inpatient initiation, like everything else in medicine, is one of balancing risk versus benefit. The outpatient initiation of anerythmic medication clearly can be done, and one of the best studies out there is actually Dr. Labreck's at full-dose SodaWall, and it can be done safely, but it requires careful patient selection, and diligent, structured follow-up. And what you have to ask yourself when you're thinking about this is do you have the time, resources, patient compliance to do this, as they are of pivotal importance to the viability of this approach. The data amplifies that one cannot predict patient compliance based on socioeconomic or income levels, and the majority of medical centers do not have pharmacy-run antiarrhythmic medication clinics. So there are clearly economic benefits to this. The DASH trial showed a cost savings of almost $4,000 per patient. But who does that benefit go to? The insurance company? The hospital? The doctor? The pharmacist? The patient? Society? We find ourselves having to often protect our patients from economic benefit. So I think that that is an issue, and how does one measure the economic savings versus the risk to the patient? Yes, that risk may be 1%, but if you're in that 1% or your mother or father is in that 1%, it's 100% to you. So what do you do with that? I think going outside black box warning and guidelines exposes the physician and the APP to significant legal risk. But clearly there are economic benefits, and clearly it's been shown it can be done safely. And I think that the only way you should dip your toe in this water is if you march this stuff out to your hospital and make the economic case that you can open beds, and if they give you enough support, these medication pharmacy clinics can support themselves financially. They're not a cost to the hospital, and they can actually help you move these patients out of the hospital. So I don't think it can't be done, but I think for most of us and for most situations it probably can't be done safely. Thanks. Thank you. Thank you very much. Well, thank you very much. Very stimulating talk from Drs. Lebrecht and Hummel. We will need to end this session about 10 minutes early, so I'm actually very pleased with their very efficient speaking. So we'll be hearing from both of them. Let me start off by asking perhaps Dr. Lebrecht whether does the patient's arrhythmia that you're treating affect whether or not you think the patient should be an inpatient or outpatient. Obviously if they've had a V-fib arrest or something, things are straightforward. But supposing they have symptomatic ventricular prematures, but that's it, or maybe right ventricular outflow tract tachycardia, does that differ from somebody with a V-fib, for example? That's a really great question. I think that in regards to the patients that are referred to me, specifically for symptomatic frequent PVCs, those patients are often coming from two different places. Sometimes they're coming from our advanced heart failure clinic if they're having CRT efficiency reductions, and they're noted to be having frequent PVCs for that. And so a crucial conversation needs to happen in regards to what is their EF? Are they on concomitant beta blockers that are so-so, obviously not being a GDMT drug? What does that conversation look like? We have had success in those patients that have had some recovery from their CRT device of their EF, successfully have suppression of their PVCs and bring their CRT efficiency back up to the high 99, 98 percentile. But in patients that do not have an implantable device and have frequent PVCs, often they are being diagnosed as an outpatient by their primary care because they get a lot of alerts from a wearable device that their heart rate is 40 or 30 and they feel fine. So that is oftentimes how patients get to our EP service and then to me as well for that suppression when metoprolol fails to suppress the frequent PVC any longer. So usually it's a risk-benefit discussion with the patient, but we have seen success with suppressive PVC therapy. In regards to other tachyarrhythmias or patients with a history of that, those discussions happen with the provider if that is a good option and what other concomitant medications we may need to adjust in that setting so that the patient can have the best outcome with minimal side effects. Before asking for Dr. Hummel's reply, I'd like to ask to sort of jump out of our fence a little bit and expand a little beyond the drugs that we were talking about. Do you really think that beta blockers do a good job in, let's say, right ventricular outflow tract tachycardias? Or is it like taking a sugar pill? Unfortunately, I don't have the best experience with that. I think it's like anything, it's going to recur, and we don't have all the answers. I think that we try to give the patient the best shot we can, and we see some success, but I think it's very patient-specific. It may make a difference that they've already begun to lower their ejection fraction too. If they're down to 25, you probably don't want to give them negative inotrope so much. Correct. Dr. Hummel? I would say that, you know, if the heart's structurally normal, we often do initiate once the agent is an outpatient. That initiation of drug is usually at a low dose, and we plan the day of initiation, and three days after that they get on a treadmill, and we treadmill them to make sure that the drug is safe. But that also gives us a sense as to how effective the drug is as well. So for those patients with the outflow tract tachycardias or idiopathic PVCs, that tends to be our approach. I would say that most of us try, you know, the mechanism is thought to be DADs, so I think that starting a beta blocker or a calcium channel blocker is reasonable. My experience has been maybe 20% of them, 30% will respond, and there's a varying degree of response. You know, typically if they don't respond to beta blocker, they generally don't respond to calcium channel blocker and vice versa. We tend to go to ablation before we go to an arrhythmic drug. So we will try beta blocker, calcium channel blocker, then go to ablation, and if it's in a tough spot or a spot that's going to require a lot of work, being fundamentally lazy, we may try an arrhythmic drug. But, I mean, all joking aside, we might, you know, when you start talking about doing ethanol ablations down the septum and that sort of thing, you may turn to an arrhythmic drug. All right. Dr. Humer, here is the online Q&A. You mentioned the IV dofetilide coming down the pipe. What's the risk of the polymorphic PMVT with the IV dofetilide? You know, I really don't know. I've just heard that there is an IV dofetilide formulation, that it's supposed to be working its way through the FDA, and that may allow us once and for all to get away from a three-day initiation. But, you know, I don't know exactly where that is, and so I'm reticent to comment on it. Anybody in the audience happen to know? Would you? Do you know? I don't. I would supplement a previous comment, too. Back in the days when defibrillators were really hard to get and ablation was in its infancy, if you treated somebody with an antiarrhythmic drug versus a defibrillator, let's say, all those trials really just tested one antiarrhythmic against a defibrillator. And you do that, it's pot luck whether that's the right antiarrhythmic. But the defibrillator is always right. It's going to stop your rapid rhythm, so it's no surprise that the defibrillator won. But the point I'm making is that when we were forced to use drugs most of the time, we did find patients who had exercise-induced VT. In other words, they'd come in with VT, we'd find an antiarrhythmic drug that made them non-inducible in the EP lab, if you can imagine. But then some of them would develop VT with a stress test, or they would have a Holter monitor with a lot of ventricular premature beats on them. So I do agree that if you're going to bet the patient's life on it, adding a stress test is a good move, and it's simple, and it's non-invasive. So another question, Megan, the patient on the road, outpatient, at home, or in a dedicated facility outside the hospital. So how did you control the connectivity issue with the wearable, at home, or the wide extended follow-up? So wouldn't it be the same as one who is loaded in the hospital, or is just a standard follow-up post-AAD? So in regards to the monitoring for the patients in the study that we did, it was a cardio-mobile device, so they had to have a Wi-Fi connection. A lot of patients that would have a smartphone were able to transmit that ECG two to three hours post-dose. If there were connectivity issues, for whatever the reason, I feel like I recall one patient that would have an issue, but she knew that that issue would be prior to initiation. So she would do her ECGs from her neighborhood library, where she had Wi-Fi access, because she didn't have Wi-Fi access at home. So she did that for three days, willingly. So one more question for you. When the study, the class 1C sartorate or patellae, how often should ischemic evaluation, or the structural heart disease, should be performed? I think that patients, upon initiation of any of these medications, should make sure they have a recent, you know, within a year, or if 1Cs, they should have it within, you know, a month or weeks, if they are just initiating, if they're new patients. But I think in regards to ongoing, I've seen patients that have had stable on their medications, you know, for 10 years or so, but maybe haven't had a recent echo. So if it's been five years, then I'm generally reaching out to our primary electrophysiologist to say, hey, can we repeat an echo in this patient, especially if the patients are unaware of their arrhythmia, and have no idea if they are in AFib, when they're in AFib, or what their rates are at that time, considering those factors, I usually recommend an echo every five years. And how many of you do the cardiopulmonary, the elective cardiopulmonary is performed in the inpatient or the outpatient? We usually will perform, if we're, if it's a class reagent, we generally will, if it's sotolol or dofetilide, we do inpatient loading. IV sotolol is generally what we use for inpatient loading, and we'll cardiovert them ahead of time so we can follow the corrected QT intervals, because it's difficult to measure the QT intervals when they're in AF. Same for dofetilide. For flecainide, it really depends. You know, it depends on age, it depends on what we're using for rate control, it depends on how rate, well the rate is controlled. Sometimes I will, if I have worries about patients developing bradyarrhythmias, or converting to flutter, I will often, I often will initiate those as an inpatient, or do a cardioversion, and then start the drug as an outpatient and have them come in for their treadmill, for the 1Cs. All right. I think the, going back to the inpatient, outpatient versus type of patient, can you, maybe I should, let's see, John has been pretty vociferous in saying that he would admit most patients, it's never all patients. And Megan, are there some patients that you would sort of look at and say, that patient, we're going to admit that patient? I definitely think that, yes, there are definitely patients that I have said that would not be a good candidate. There have been, you know, those rare patients that have, they don't have a rapid ventricular response when in atrial fibrillation, they have a slow response, which I know isn't the norm. And so I've had a patient or two referred over for outpatient initiation, but their response is slow. And so obviously I felt that that would have been very inappropriate to start a patient on something that would suppress their, you know, AB node at the same time. And so I recommended to their primary electrophysiologist that referred them that it would probably, they would most likely need a pacemaker to support antibiotic drug usage for their AFib treatment, which ultimately the patient got and then came back for outpatient initiation. Do we have questions from the floor? A little bit overlap. Are there questions from the floor while we're scratching our heads up here? You can use the QR code or you can come to the microphone. Multi-source access. I actually put that in the thing, but I guess you can't see it. The question is regarding pill-in-the-pocket testing. What is it that we're looking for? The patients are often in sinus rhythm at that time. Other than the extremely rare possibility of a brugada pattern, what are you expecting to see? In those trials where they had adverse effects, many of them are conversion to flutter, to slower cycle lengths of flutter so that they're conducted rapidly through the node. And even though they were on beta blockers or calcium channel blockers, they still conducted rapidly. The other group was primarily bradyarrhythmias. The patients will start their diltiazoma or their topral 45 minutes or an hour ahead of time and then pop in the flaconide and they convert and they come in with sinus arrest or they have complete heart block in the ED. That number was anywhere from 6 to 15%, which is a pretty big number. The recommendation isn't that every time they take the pill-in-the-pocket, they've got to come in. It's just for their first trial, if you're going to... And what we generally will tell them is, look, if you go into AFib, go to the ED and tell them you've got this regimen and you're supposed to start it there. And at Ohio State, they'll start it in the emergency department. Our emergency department doctors will give them the regimen. It's in epic so they can see our plan. And then if they do well, they kick them out. So you wouldn't prescribe pill-in-the-pocket to a patient with paroxysmal AFib. They would have to come into the ER and get their first dose in the ER. I'll prescribe it and I'll say, look, okay, here's the regimen. You've got to come in. Either call us and tell us you're in AFib and we'll put them in our IPR or as an inpatient for a few hours and have them start it. And then if everything looks okay, then they can leave. Thank you. All right. Next. Is that just for the first time they do it? Yeah. And then if it looks good... Subsequent events, they do it at home? Yeah, all the subsequent pill-in-the-pockets, they take at home because they've proven themselves to be okay. Hi. I'm Rachita Navara, EP from San Francisco. I'm so glad that there's a session on this. This was such a pain point of mine, treating patients with antiarrhythmics, that I actually created software to help monitoring of QTC for patients in various settings. Our experience in my own private clinic has been that we are able to catch instances of noncompliance, for instance, with QT shortening for patients who are supposed to be on class 3 antiarrhythmics. And that has helped us identify that this may not be an ablation failure or a treatment failure, but maybe a compliance issue. And certainly for medications like flecainide, we've had instances where under a traditional protocol, if we just had a patient come back and do a 12-lead a week later, we may not have caught. Instead, we were able to see pretty immediate QRS with increase during this monitoring period, pairing with devices like loops, et cetera. And so I was curious, for many of you on the panel, if this type of software would help your workflows, or if there are other pain points that you've encountered. This is my own personal research focus, and we have three NIH grants on this, so I'm super interested to hear. I mean, I, you know, there were, at the bio-design yesterday, there was a whole bunch of stuff about prediction, about catching ventricular arrhythmias. And, you know, you look at the march of AI being able to tell us if QT intervals are getting out of range. It might be a hint that these patients, once they leave Ontigasin, that their renal function is going down. You know, there's a lot of room, I think, for software development in here. And there's so much information that's coming at our pharmacy clinic. Anything that can help them, I think, would be a benefit. I agree. I think there's a lot of information to sift through. I think there's a lot of, you know, laboratory data that we, you know, monitor per the guidelines. I think that there's a lot of drug interactions that we don't catch because it's not reported through the software that our EMRs, you know, talk to based on, you know, like coupons, like GoodRx, which don't communicate with, if it's not through your insurance, it doesn't get reported through the, like, SureScript software for EMR. And so I think detections that we may not see on a 10-second ECG in the clinic would be important for something like this to, you know, pull out and parse out that information. So I think that software is really, that would be really important for our patient population. I think we always forget, I think it is easy for us to forget because we do it every day that this is, aside from chemotherapy, one of the most toxic and fatal drug classes that we can prescribe. And so I think that that slide that you shared about how, like, how, what percentage of people follow the guidance and monitoring is a little scary, actually, because, you know, patients may do a completely, you know, don't call about interactions, don't call about, you know, recommended changes, things of that nature. So, I mean, I've seen patients, you know, that not, haven't gotten blood work for years, and then they come back in there in, like, wild AKI and surprised that they're alive. So. All right. Thank you. One more question, maybe. So before the last question, okay, I'd like to ask you, I'd like to know your idea. Do you practice parents? So outpatient raise hand first, and then inpatient after. Okay. Outpatient. Okay. Thank you. And then inpatient. What do you think? Yeah, I think very interesting. Thank you very much. But I think the weight was tilted towards inpatient. Yeah, right. Maybe 60 versus 40 percent, just a glance. My vision is not clear, but. One of the things, there are a lot of aphorisms that, you know, wise sayings that come from that. One of my colleagues has pointed out that one good thing about a device is you don't have to remember to take it every morning. It just works. It's sort of like shoot and forget. All right. I'm from New York. I want to thank both John and Megan to cite my paper, actually. But additionally, I think the outpatient initiation, dofetilide and Sotilol, important dofetilide, we devised during the COVID time. There were so many other situations, and they couldn't go to hospital for ablations or cardiovascular and whatnot, and carried on that protocol. So having said that, you know, I still admit patients for inpatient dofetilide admissions. And the question is, you know, when you go from, say, 250 BID to, say, 375, just increment by 125, are you going to admit the patient just for one small dose increment? Although they may have defibrillators or pacemaker or some other device to check on the QTCs. So I think that's the main questions that I still struggle in my mind, and I still admit them. I just want to know what your views are, John and Megan. I'll go first. I mean, you know, I can barely get through my in-basket in my EMR. I'm not going to, I, the odds that I'm going to be on time to monitor this patient's QTC and have them, you know, if I don't have a Megan Labreck to monitor this for me, then they're coming in. It's just the reality of life. I'm not, I don't, you know, obviously a lot of it depends on their baseline QTC, their willingness to come in. You know, if they stomp their feet and refuse and say, you know, I'm willing to take all risks, you know, maybe I'd give it to an outpatient. In my day, I just am too busy to be bothered with it. They can eat bad food for one evening and be, or for a couple evenings and be uptitrated. And, you know, it's just because I don't have a way to do that safely for them. My first thought is why would you, why are they not on that optimized dose in the first place? Did they fail it? Did they have to be down, dosed down initially because of QT prolongation when they were initiated in the first place? So that's my first concern is an uptight, like why are we uptitrating something that they may have not already tolerated? So the risk of QT prolongation in that setting, but if they didn't get initiated on a higher dose ever, then I would recommend bringing the patient in unless you have a means to very, very closely monitor that patient. But I usually, I would favor bringing a dofetilide patient in. I think the risks are too high. Well, I think that we've had a fairly rousing debate here dealing only with a couple of classes of drugs, you know, the 1Cs and some of the 3s. If you expand that to other modalities, I mentioned ablation, there are devices. Quinidine is making a comeback for a number of things. Maxillitine for certain drugs can, we find, at least be a really great adjuvant for lower dose amiodarone. There are all sorts of combinations that we didn't get a chance to cover, and it does emphasize the need to follow patients carefully, including things like changing renal function. The patient is going down a little bit, and their GFR is 40. I would think twice about starting them on dofetilide at that point. So we've learned a lot, we've heard a lot, and we've learned, I think partly, that there's a lot more to learn. Dr. Kim? Thank you very much. You're a great participant. Thank you.

outpatient loading

inpatient loading

antiarrhythmic drugs

torsades risk

patient safety

healthcare efficiency

FDA black box warnings

dofetilide

sotalol