to our session on arrhythmias in pregnancy, which follows the recent publication of the scientific statement, which all the members of this panel have been strategic parts of in different ways. For the purpose of the session, please use your mobile app to actually be able to offer questions that we'll go through for Q&A at the end of all the talks. So our plan is to kind of introduce each of our session speakers, go through each talk, and then at the end, we'll go through each individual questions that you may have. For the purposes of the actual conversation, we want this to be interactive as much as possible, so either the app or we have a microphone in the corner there, so please also feel free during the Q&A session to get up there. So to start, I'll actually start by introducing my co-chair, Dr. Jose Joglar, who's going to be going over the first talk here from UT Southwestern Medical Center. Good afternoon, everyone. Thank you so much for being here today. I'm Jose Joglar from UT Southwestern. And we're gonna start by giving an overview of the incidence, pathogenesis, and diagnosis of arrhythmias in pregnancy. To my disclosures. So I'm gonna use, I'm gonna be referring to this document, which is, like Suresh said, the 2023 Expert Consensus Statement on the Management of Arrhythmias During Pregnancy, and I'm happy to report that most of the group here, of the speakers and the co-chair were member of the writing committee. So as a matter of introduction, when arrhythmias occur in pregnancy, two lives are at risk. First and foremost, the care of the pregnant woman should not be compromised for fear of providing needed treatment in pregnancy or potentially exposing the fetus to risk, since restoring of normal hemodynamics is the priority. Restoration of normal hemodynamics is the priority. Thus, the overall approach of the treatment of arrhythmias in pregnancy should be largely like the approach in non-pregnant patient with some exceptions. I'm gonna just discuss incident pathogenesis and diagnosis, and then the other speakers will talk about treatment. So in general, there's an increasing incidence of arrhythmias during normal pregnancy. Most of these arrhythmias are mainly PACs, premature atrial and ventricular beats, which is very, very common finding, seen in 50 to 60% of pregnant patients. The number of simple PVCs is higher Non-pregnant patient also can have a lot of PVCs, so the prevalence of PVCs in general is not that different, but the number of them is higher in patients with pregnancy, during pregnancy. I have to say, though, a lot of patients have symptoms that are often, most of the time, symptoms of palpitations correlate with sinus tachycardia. In fact, only 10% of the symptoms of palpitation in pregnancy are correlating with arrhythmia. So it's very common, the reporting of palpitations. What about the effects on supraventricular tachycardia? This is a study by Lee many years ago. 207 patients diagnosed with PSVT. They had questionnaires, and even though the first onset of SVT during pregnancy was rare, the fact is, those patients who have already an underlying substrate, who already have a substrate for SVT, have an accessory pathway, or dual AV nodes, tachycardia episodes were very much more common during pregnancy than in the non-pregnant state, and this has been also reported for right ventricular outflow tract tachycardia, as with the patients during pregnancy, especially in the last trimester, tend to have an exacerbation of episodes. This is, we're starting to see data. This is from my own institution at Parkland Hospital, where you can see that the majority of arrhythmias, by far, tend to be reported arrhythmias, sinus tachycardia, sinus bradycardia, or sinus arrhythmias. So the great majority of arrhythmias in pregnancy tend to be benign, but certainly, there is a possibility also of, and also PACs, PVC, but also there is a possibility, an increase in frequency in recent decades of more serious arrhythmias. Sorry about that. And you can see here, this study is quoted frequently, and this picture I took it from the 2023 statement. You can see that there have been a frequency per 100,000 pregnancies of, and age groups increase frequency of arrhythmias. In part, it's because a pregnant woman with, they tend to have, these days, they tend to have, reach a maternal age later in life, but also patients with, for example, congenital heart disease now can reach a maternal age, and things like that, so longer survival of patients with significant underlying heart conditions, and later age of pregnancy, and other things, have shown here that then you have an increased incidence in recent decades of atrial fibrillation, and that is probably the most common sustained arrhythmia. Like I said, most arrhythmias are benign, but atrial fibrillation, or SVT and VT, are increasing in prevalence. Potential mechanisms might be, for example, the most important pregnancy-induced cardiovascular changes, increasing blood volume, cardiac output, stroke volume, heart rate, decreased vascular resistance, pregnancy-induced increases in estradiol, progesterone, free cortisol, also the autonomic level in pregnancy progresses. There is a shift from vagal to higher sympathetic milieu, and then more frequent ectopy that I already mentioned. Don't forget that in patients with a arrhythmogenic substrate ectopy tends to be a trigger for sustained episodes. So when it comes to evaluation, it should be the same as in the non-pregnant patient, with the exception, perhaps, of some very specific syndromes that I'm just gonna touch upon. But in general, for the great majority of the population, it is the same. I just wanna also point out that a lot is being said about the heart rate that increases during pregnancy, which is true, but this study, I like, because it was kind of a meta-analysis of 39 studies that evaluated the blood pressure and the heart rate of pregnant women throughout pregnancy, throughout the different weeks of gestational age. And you can see that commonly thought substantial decreases in blood pressure mid-pregnancy were not seen, and they also, the heart rate increases in pregnancy are real, but not as high as previously thought, and this is very important. When you look at all these studies, they saw a 7.6 heart rate, bits per minute, during pregnancy increase. This is very important because we have to be careful not to miss atrial tachycardia. Sometimes an atrial tachycardia can, focal atrial tachycardia can come, originate from the hybrid atrium, high near the sinus node, can confuse the picture, can be, can look like sinus tachycardia. It can have even changes in heart rates, but it might be an atrial tachycardia putting the patient at risk for tachycardia-induced cardiomyopathy. When it comes to syncope, syncope is fortunately rare during pregnancy, 1%, which is kind of same as the general population, vasovagal, same as the general population, being the most common. So again, syncope is the same as the non-pregnant state, except for what is called the supine hypotensive syndrome, which is unique to pregnancy. Eight to 11% of women develop a greater than 30 millimeters systolic blood pressure drop with or without symptom with lying supine. Symptoms may include dizziness, nausea, in rare cases, syncope. And MRI studies have shown that gravid uterus begins to compress the inferior vena cava in the supine position, beginning with the 20th week of pregnancy with severe obstruction at term. And this is what you see. This is a study of MRI, where you compress the vena cava here with the uterus, where if you displace laterally, then you decompress the vena cava. So again, syncope, lightheadedness, dizziness, the same as in non-pregnant state, except in these possible situations, you need to recognize patient's laying down and might feel uncomfortable, and the treatment is to turn the patient to the side. When it comes to prognosis, I just wanna emphasize that arrhythmias are not benign. There's, like I mentioned at the beginning, there are two lives at risk. The priority should be to restore normal hemodynamics. This is a study here showing pregnancy outcomes for example, in patients with SVT, paroxysmal AFib flutter, AFib becoming now increasingly the most common sustained arrhythmia requiring hospitalization in pregnancy. VT, and you can see an increased incidence of adverse fetal outcomes. Of course, there's always a possibility of some of these outcomes are caused by a pre-existing substrate, for example, cardiomyopathy in patients with VT, but if you look at this most recent study that look at potential complications in patients with supraventicular tachycardia that pregnant women were otherwise healthy, you can see that that study also show an increase in adverse effects for the fetus. For the fetus, okay? So there was odds of cesarean section, which I don't take very seriously because that can be elective, but there was an increase in odds of pre-term labor for sure. So even in very, very healthy people, pregnancy needs to be tackled promptly, accordingly to avoid complications. So in conclusion, pregnancy is associated with increased risk of arrhythmia, especially in patients with a pre-existing substrate. The most common arrhythmias in pregnancy are generally benign, including sinus arrhythmia, supraventicular tachycardia, premature beats, where life-threatening arrhythmias such as hemodynamically significant SVT or VT are less common. Atrial fibrillation has become increasingly more common in research years. Evaluation should be for most part as in the non-pregnant state, and the other speakers are gonna be telling us a little bit about management. Yet clinicians should be aware of some syndrome specific to pregnancy, such as supine hypotenuse syndrome, and also don't forget the possibility of atrial tachycardia that might look like sinus tachycardia can lead to atrial-induced cardiomyopathy. Thank you so much. Thank you so much. Thank you, Dr. Duglar, and again, please use the HRS app to have any questions which we'll address at the end. Now it's my pleasure to introduce Dr. Alexis Tomolo to talk about the medical management of arrhythmias in pregnancy from the University of Colorado. Thank you so much, Dr. Kappa and Dr. Yogar. I'm really delighted to be here. All right, with that background, we'll move forward. So really quickly, just industry disclosures, but also I just wanted to show this slide because I am a mom, too, and was pregnant during the end of my fellowship doing this complex congenital case while a couple of my fellow attendings were in the control room and our fellows were out there as well. But just to show that we're in this field where it is difficult to kind of manage your family and still be in the invasive space, but it is totally doable, so for trainees out there, happy to talk to you. But this topic is important to me in a lot of ways. First of all, U.S. maternal mortality rates have doubled over the past 20 years, which is very disappointing. And the greatest impact has been on certain groups, patients in lower socioeconomic groups, but also certain racial groups as well. And cardiovascular disease is still the leading cause of pregnancy-related mortality with hospitalizations for arrhythmias being associated with maternal and fetal outcomes, as Dr. Yogle just demonstrated. Risk factors for arrhythmias in pregnancy include increased maternal age, which we're seeing that more commonly, but also these lower socioeconomic groups, and underlying cardiovascular diseases, including adult congenital heart disease as well. So this really impacts a lot of our patients and we can all work together to provide better outcomes for a lot of folks. So today what I'd like to do is help us construct a comprehensive team for pre-, peri-, and postpartum arrhythmia care, recognize underlying cardiac conditions that could increase risk of arrhythmias in the peripartum period, recommend safe antiarrhythmic regimens for pregnant and breastfeeding patients, and identify safest anticoagulant regimens for patients with the highest risk factors for thromboembolism in pregnancy. We're gonna do that through some cases because it's the end of the day. We need to wake our brains up a little bit. So this is a 34-year-old lady who was G3P2002, so in her third pregnancy she had two term pregnancies that were both living. And she was referred to me at the very end of her pregnancy at 38 weeks to establish care. She was from Central America and had no prior records, but what I heard was that she had Brugada syndrome, had had uncomplicated prior pregnancies and vaginal deliveries, had cardiac arrest a year ago, and was on a beta blocker but had no ICD. So there were a lot of things that didn't quite make sense. And I saw her in clinic and this was her ECG, which really did not fit any criteria for Brugada, and so brought up a lot of questions. But what are we gonna do at the end of her pregnancy? We really need to think about working together as a team to reduce any risks of arrhythmias during her labor and delivery. So this is just kind of some of the folks who might be on a maternal fetal heart team, so thinking about working with your MFM group, OB anesthesia, neonatology, your cardio OB team, including us as electrophysiologists, genetics, pharmacy, also pediatricians. And what we do together, and in our institution we have meetings every couple of weeks where we talk about all of our pregnant patients who kind of fall into these high risk cardiac categories. But we think about care optimization, but also pre-conceptual evaluation, say for our ACHD patients who are considering pregnancy. But also go through emergency planning and specifics of the birth plan. So is a patient okay to labor? Should they have a cesarean delivery? What medications should we avoid or minimize? And that's a huge one for us. How should we manage their anti-arrhythmics and also their devices if they have any? Do we need to reduce catecholamines during labor? And what should we think about after delivery too? And that includes medications that can be used with lactation or ones that should be avoided. Fortunately our patient had no evidence of Brugada on any of her ECGs throughout her whole course. She was continued on her beta blocker just because she was doing well with that already. We talked about doing genetic testing and some further workup to kind of see what actually led to her cardiac arrest after her delivery. But we did give some recommendations as backup plans for if she had ventricular arrhythmias, including having isoproteranol or quinidine on hand, which are not common medications on the labor and delivery floor. Thinking about avoiding certain medications. And she did very, very well. So this is just an illustration of that, that we have this comprehensive team that's not just there at the time of delivery, but we need to think about our patients afterwards and also prior to pregnancy too. All right, what about patients who have cardiac conditions that might increase risk of arrhythmias in pregnancy? So a 24-year-old woman who came in to see me for preconception counseling. So she wasn't currently pregnant, but had had a child previously. She was diagnosed with lung QT1. So she was diagnosed at age 11, and this was in competitive soccer screening. She had a cousin who died suddenly during basketball. And she was actually, she's very active. She was active her whole life and did very well on beta blockers. She had an uncomplicated first pregnancy four years prior and delivered by cesarean delivery. So she was maintained on propranolol without any issues and did not have an ICD. This was her ECG when she met me. And actually her baseline QTC was not terribly long. It was 466 milliseconds. But I bring this case up as one where we gave specific recommendations, especially to our OB anesthesia team about medications that they might want to be careful with during her labor and delivery. So I wanted to highlight a few of those conditions that we think about. So Brugada syndrome, like my first patient, I give the advice to reduce bupivacaine, which has been shown to unmask Brugada pattern on ECG, but also has been associated with VT and VF in patients with Brugada. Avoidance of propofol and treatment of fevers, particularly mastitis, has been shown to unmask Brugada previously. In lung QT syndrome, we do try to continue beta blockers through pregnancy. And also think about the postpartum period, especially in lung QT2, where there is a higher incidence of ventricular arrhythmias postpartum, and that can extend up to nine months postpartum. For lung QT patients, especially who've had ventricular events previously, thinking about reducing catecholamines, and that might be with providing an assisted second stage of labor. And some caution with certain anesthetics and telemetry monitoring. Arrhythmogenic cardiomyopathy, such as ARVC, they actually do pretty well during pregnancy and delivery, but we're often continuing antiarrhythmics when we're able to during pregnancy. Catecholaminergic VT, as the name suggests, you know, is one that we want to be thinking about reduction of catecholamines, especially during labor. And lastly, hypertrophic cardiomyopathy. These patients also do very well during labor and delivery, but thinking about reducing catecholamines for them, but also thinking about the other parts of the physiology that happens for HCM patients. That we want to monitor their preload, give fluids if we need to, and have caution with spinal anesthesia because that can reduce your blood pressure as well. I think it's important to just think about thoughtful device management. For example, a patient with a subcutaneous ICD might have abdominal contractions that lead to over-sensing on their devices, and that might lead to shock during labor. So that's a time when we would disable the tachytherapies on an ICD, but that's not necessarily the same for a patient who has a transvenous device, and so you have to really think about the patient who's in front of you, and keep an eye out for the baby who's coming forward too. So my patient with long QT actually had her course complicated by severe preeclampsia. They needed to switch to labetalol. She was able to have a cesarean delivery and delivered a healthy little one, but had a very long QT the second day after she delivered at 573. So we also gave advice about careful electrolyte monitoring and repletion, and quickly got her back to propranolol, which was okay for her to use during breastfeeding. That brings me to the next topic of medication management. So this patient, this next one, is a 27-year-old woman who's had palpitations for the past nine years, and now she's 13 weeks pregnant. She has a structurally normal heart, and she is developing more frequent symptoms of palpitations requiring a lot of ER visits where she was given adenosine. This was her ECG, which was consistent with typical AVNRT, and so a question that came up from her case is, which antiarrhythmics are safe? Is it okay that she got adenosine a whole bunch of times? And so the moral of the story with antiarrhythmics is a lot of what we do in our non-pregnant patients is okay to do in our pregnant patients, with some exceptions, but the, you know, first and foremost in acute management, we are thinking about safety of mom. And so if we have a patient who's hemodynamically unstable, we should cardiovert them, and thinking about thoughtful placement of pads during that to avoid breast tissue. For folks who are hemodynamically stable, we encourage the same sort of protocol that you would do for a patient with SVT who wasn't pregnant, starting with vagal maneuvers and adenosine. Beta blockers are kind of preferred, as well as verapamil is a calcium channel blocker that we do prefer, and then some of these other medications as last resort. And for chronic management, we really lean on beta blockers for a lot of our pregnant patients, where we're really monitoring for intrauterine growth restriction with these, but those incidences of significant intrauterine growth restriction are small, and if we're moving on to other antiarrhythmic therapies, we're thinking about flecainide and propranolol, which have had more observational data for safety for our moms. For my patient, we gave her metoprolol during her pregnancy. She had an increased frequency of growth ultrasounds, and she did great during her delivery, and then we went on to ablation for her. Wolf-Parkinson-White sometimes is a little bit of a different beast, and for these patients with WPW, it's okay to use ibutylide or procainamide IV, and chronically flecainide and parpafinone. In VT, we're thinking about a lot of the same medications for acute management as in SVT, IV beta blockers, adenosine, verapamil, and lidocaine would be our next choice there. Procainamide, a little bit less so for the risks of associated development of lupus, and in chronic management, working again with beta blockers and flecainide, parpafinone, sotolol mostly, a little bit less so quinidine and myxilatine. I really like this graphic from Dr. Temerisa from 2022, which highlights some of these buckets where we prefer those agents over other agents for medical management of arrhythmias, and what this shows, too, with an extra picture is, is it okay in lactation? That's a really nice resource, along with the wonderful 2023 guideline. Very quickly, this is a patient that I'm going to meet next week. She is a 46-year-old lady who has a history of an unprovoked DVT. She's on a chronic DOAC, and she was recently diagnosed with paroxysmal AFib, with an increasing burden on her most recent monitor, who's thinking about hormonal therapy for in vitro fertilization. This is her current ECG, and it just brought up the question in my mind about whether this is a patient that I would think about anticoagulating during her pregnancy, and what the best choices would be. Oftentimes, we're using anticoagulants when people have a very high risk of thromboembolism, and those are folks who have, say, rheumatic mitral valve disease, mechanical valves, but also we have to think about the fact that the CHADS-VASc does not really bring in the high thrombotic state of pregnancy, so thinking about weighing that risk, along with a risk of intracranial hemorrhage for the developing fetus. Most often, we are working with the heparins during pregnancy and breastfeeding, lovanox outside of the hospital or heparin drip within the hospital, and when we are working with warfarin, trying to limit that dose to five milligrams or less, we avoid it in the first trimester as well because it's teratogenic. The DOACs have not been shown to be safe in pregnancy yet, and so those are avoided at this time. So just to summarize, we want to work with our whole team to provide the best care to our patients with arrhythmias during pregnancy, recognize certain cardiac conditions that can increase risk of arrhythmias in the peripartum period, and think about their own physiology and how that might affect what medications we would or wouldn't want to use. Think about the most effective antiarrhythmic regimens that we can use safely for our pregnant and breastfeeding patients, and also identify the heparins and lotus warfarin as the safest anticoagulant regimens. Those are some of the papers that I use the most for this, and many thanks to everybody. Thank you so much. Thank you so much. Thank you so much, Dr. Mollo. Next, I'll be introducing Dr. Tess Sorrell, talking about fetal arrhythmias in pregnancy. Thanks very much for the terrific talk so far, and thanks for inviting me to here today to speak to all of you. So I'm excited after hearing the most recent talk. It reminds me we're starting to get a little bit of more data in pregnancy. I think this document spurred that. I know it did, because I started telling friends, I'm like, yeah, we have no data. We have no data. And then, you know, we all want to publish, so this is great. So fetal arrhythmias. The normal fetal heart rate is actually between 110 and 160 beats per minute. So faster than, I mean, sorry, slower than most newborn heart ranges, or a little bit narrower than newborns. So if the heart rate's beyond the normal range, or the rhythms are regular, then we detect a fetal arrhythmia. And it's also possible to have a fetal arrhythmia that's in the normal heart range and is regular, but those largely go undetected until birth, because we don't have EKGs to look at in fetuses, and so we're not going to diagnose a natural tachycardia, or even a slow VT, that's it, unless we hear an abnormal heart rate. The heart rate, the duration, the mechanism of the rhythm, and the degree of irregularity usually predict the consequences, and it's pretty common in the world of pediatric cardiology and congenital. One percent of all fetuses we would consider relatively common. So first thing that happens is when OBs hear a heartbeat that's fast, slower, or regular, they suspect arrhythmia. And the diagnoses are actually made largely by echo. It counts for about half the referrals for fetal echocardiograms, which is interesting. Some lucky centers have fetal magneto-electrocardiograms, like Jeanette sitting here in the audience, but it's very expensive technology and most of us don't have this. We would love to, but most of our hospitals will say it doesn't justify the cost. So we are using echo, and so here's an example of a baby we treated recently, a little girl, baby X, who came in, had a heart rate detected that was fast by the OB, and she was sent for a fetal echo, and she actually has high drops. So this is what it looks like by echo. You have extracellular fluid collection, and you get ascites, you get pericardial effusions, you get pleural effusions. So it's basically fetal heart failure. When we count the heart rate, again we don't have an electrocardiogram, so we're using different forms of Doppler to count the heart rate. So here we're looking at, you can either use inflow or outflow, and we count the V to V rate. In this case it was about 189 beats per minute, when this baby was consistently in the round 190 is what we were getting. You can also use M-mode to look, it's a nice way to look at AV relationships to see if they're one-to-one or not, and you can do kind of a long quote-unquote rhythm strip with M-mode, and this baby had one-to-one tachycardia. So we put the Doppler through the atrium and ventricle in the wall and look at wall motion. Here's an example where we're looking at using our Doppler signal. This baby had a quite a long PR tachycardia, but you can look at things like short PR or long RPs. So you can use Doppler for a lot of, you have to be, takes a while, it's not easy, but you can get a good diagnosis if you spend the time. You can also look at flutter. So here's an example of flutter with M-mode where there's more atrial contractions about in the range of flutter rate, and it's about 2 to 3 to 1 in this baby for flutter. And VT, usually you have more Vs than As. So you do need to spend time and make sure you get the right diagnosis because if you don't have the wrong diagnosis, your treatment's wrong, and I've seen that happen with bad outcomes. Okay, so I'm just going to run through a few highlights that are interesting to me from the document. So this is a recommendation that comes along frequently in this document. I just want to point out that phone a friend early, call your cardio obstetrics team, as we just heard about, because they deal with this all the time, whereas a lot of us deal with it rarely. If a baby's in VT, with or without hydrops, and they're close to term or near term, go ahead and deliver. So those are common recommendations throughout the document for fetuses. No, you don't think so. We'll get some good questions, but that's a generalization. If a baby or a fetus has sustained VT, with or without hydrops, and they're not mature enough for delivery, then you start to treat the mom. So you're treating the fetus transplacentally with either IV mag or propranolol, myxilatine, or lidocaine, or in combination, depending on what we think is the etiology. And then we have to look for fetal well-being and maternal toxicity always, because you're using high doses of drugs in mom. These recommendations, again, level of evidence for fetuses are generally B and C. So we have no positive randomized controlled trials for this. Second interesting thing to remember is if a fetus has sustained VT, correct mom's hypomagnesemia, her mag, if it's there, and sometimes we forget to do that. A 2A recommendation for VT, if the baby has hydrops or a ventricular dysfunction, and the baby has been refractory to treating mom with high doses of medication, it's a 2A recommendation to move on, if they don't have inherited arrhythmias syndromes, to transplacental treatment with flax, sotolol, or amnio, and it can be beneficial. And you have to pick which drug depending on risk-benefit profile for the mom and the baby. Moving on to bradycardias, picking out a few choice facts here. In pregnancies complicated by unknown reason for fetal bradycardia, please don't forget to check the baby after birth. These might be undiagnosed inherited arrhythmia syndromes, particularly long QT. So don't forget to refer that baby to pediatric cardiology, you know, even if it's just, we need an EKG after birth, because we can't diagnose that in utero a lot of the times, unless you're in a setter with, like, Jeanette's with magnetocardiography. So other interesting recommendations, 2A, we have a recommendation that if the mom has anti-Rowan law antibodies, check the baby for heart block continuously. It's reasonable to do this throughout pregnancy, to look for development of first, second, or third degree heart block, and also for cardiomyopathy, because some babies develop cardiomyopathy even if they don't get the heart block. Some 2B recommendations, so steroids, fluorinated steroids may be reasonable to give after shared decision-making with mom, but the pros and cons, they tend to be relatively low risk, although there's some data saying, that's pretty good data, saying that they may not work, but the risk is low. The other 2B recommendation in this section is that if there's heart block, secondary to maternal isoimmune disease, and the baby's getting into trouble with cardiomyopathy or hydrops, giving the fluorinated steroids and IVIG may be considered, discussing the pros and cons for the mom and the fetus. And finally, we have a class 3 recommendation in that if the baby's heart rate is less than 55, that's sort of a cutoff where we all get really nervous that this baby's not going to make it to term and may develop hydrops, please don't use beta agonists. They don't work. Okay, so just a few points about long QT syndrome. Some class 1 recommendations. So if the mom or the baby are suspected of having inherited arrhythmia syndromes, you should actually look at the heart rate carefully because that, if it's low, it usually indicates the baby's affected. If there's torsades de pointes, go ahead and load IV mag for mom. It works, and that should be first-line therapy for long QT. If they're suspected or documented maternal or fetal inherited arrhythmia syndromes, avoid medications that are contraindicated, and we heard that earlier today. A 2B that's interesting is magnesium's reasonable at all stages, even if before you go to delivery, if there's some torsade in the baby, in the fetus. So even, so this is the one case where you might not deliver right away, you might try some mag first. And then a class 3 is, if they have torsade or polymorphic VT, you got to avoid soteloprocranibinamide, you know, just like you would in older patients. Okay, and finally, SVT is the most common rhythm that we're going to see. We define incessant arrhythmias as more than 50% of the time and intermittent as less than 50% of the time that the baby's in the rhythm. So that's the definition. If they've got SVT or flutter and they're not ready for delivery, not mature enough, then you treat mom with flaconide or sotelol, often in combination with ditch. And you choose your your meds after talking to your cardio obstructive team about the risk-benefit profile. Some other interesting one, class 1 recommendations are, if you have a fetal irregular heart rate or tachyarrhythmias, always go to fetal echo to look for congenital heart disease that may associate, be associated with SVT. There's a higher rate of SVT in congenital heart disease, so look for that on the echo. And then PACs, follow the PACs. They can lead to SVT down the road, so just don't always say goodbye if there are a lot of PACs in the fetus. 2A recommendations, I'm going to get moving here, but first-line for incessant SVT, that's refractory to first-line drugs. you can move on to either oral AMRIO, so AMRIO is considered a 2A because of the risk profile, and, or transplacental use. If you're gonna move on to transplacental treatment, you really gotta go to a center that's highly specialized in this treatment, because it's risky. 2A, 2B, I'm sorry, recommendation is Flutter, and SVT that's incessant, and there's hydrops in the baby's preterm, consider more aggressive therapies, again, at a highly specialized fetal heart center. And finally, don't use verapamil for transplacental therapy. It inhibits cardiac function in the fetus. Okay, so briefly, here is baby X. We treated with flecainide and DITCH in the mom, and lo and behold, the heart rate went down to 150. Hydrops resolved, so this is a happy heart. No more fluid collections in the baby, and looking good, so we were all happy. And to summarize, fetal echoes are the primary method for diagnosis of fetal arrhythmias. Phone a friend early and often, your cardio OB team. Early delivery may be the best option versus medical therapy in pregnant patients if they're near-term, because a lot of these meds at doses we use can be toxic. And direct medical therapy to the fetus is very risky and should be done only by experienced centers. And then always make sure you get the diagnosis right. So is it VT or SVT? Is it Flutter versus one-to-one SVT? Is it long or short RP? Also, sinus bradia versus AV block. I mean, make sure you get the brady diagnosis right, or is it just blocked PACs? Because it's much harder to make the diagnosis in fetuses because we're using echo and not EKG. All right, and thanks to the rest of the chairs and the committee members on this document. It's been great, so thanks very much. We'll take questions at the end. Thank you. Thank you, Dr. Sorrella. And it's my pleasure to introduce the last presentation of this session, Dr. Jennifer Wright, who will be talking about cardioversion and invasive treatment of arrhythmias in pregnancy. Well, Dr. Wright, get ready. We have a few questions here on the question electronic, so we'll try to get to a few of those at the end. All right, well, good afternoon, everybody. I'm Jen Wright from the University of Wisconsin, and I get to wrap this up by talking about invasive treatment of arrhythmias in pregnancy. So three objectives. We're gonna be talking about, first, the data, and then how to, with performing cardioversion, ablation, and device implantation during pregnancy. So let's start with cardioversion. I thought it would be best to do this with case reports. So this is a 35-year-old female. She has a history of non-ischemic cardiomyopathy, and she's coming in hypotensive and symptomatic from cysteine VT. So what is the best next step? Do you give IV adenosine, DILT, do you cardiovert her, or do you call OB and just wait to see what they say? So I think we've heard this already multiple times today that restoration of normal maternal hemodynamics is the priority. So the answer is cardioversion, or shock, you will. So because cardioversion is overall safe and it is effective. Now, as the prior speakers have alluded to, a lot of the data that we're talking about when it comes to management areas in pregnancy are level of evidence C and limited because they're based upon retrospective data and case reports. But fortunately, a lot of people have published their experience with this. So one group accumulated about 46 case series on the use of cardioversion during pregnancy, and there was a paucity of adverse effects, yet it was also successful. Another group then looked at umbilical blood flow, pre and post cardioversion and showed there's no change. So very reassuring. And of note, in that study, they used the typical doses that one would give for management of SVT. So when we go to that 2023 document that we've all been talking about earlier today, when it comes to cardioversion, the first thing, even though it's based upon level of evidence C and limited data, it's a class one recommendation to cardiovert the patient. You have to restore normal maternal hemodynamics. It's also important to note how we place the electrodes because if we're gonna place electrodes on breast tissue, we have something in the path. So we want that path to be a straightforward path between our electrodes, thereby decreasing the impedance and thereby increasing current for a given amount of output. So when you are placing the patches, it's important if you're dealing with a ventricular arrhythmia, either sternal apical versus a supraventricular arrhythmia, put anterior-posterior and just making sure to avoid the breast tissue as much as possible to get that current delivery that you need. So going back to our patient, what's the best next step? It's not doing that. So we don't wanna call any pots. So we go ahead and cardiovert that patient. All right, let's move on to ablation. So this is a patient who came to me at 17 weeks of her pregnancy. She's 26 years old. And she came to me with this ECG, which clearly shows manifest pre-excitation. And she was presenting with palpitations and syncope. So if we were to ablate her, which of the following are not true regarding ablation therapy for this patient? Minimizing or eliminating fluoroscopy is recommended. If fluoroscopy is used, the fetal dose is actually lower than that of the mother. She should actually just wait and pursue any treatment until she's done and she delivers her baby. Or ablation planning should be multidisciplinary. I think we've heard this before as well today. So the 2017 EHRA consensus document on occupational radiation exposure in the EP lab does a nice job talking not only about the radiation safety of workers in the EP lab, but also with pregnancy and the patients themselves. Because they list the average radiation exposure for most EP procedures. And I thought this was very helpful in knowing where we are if we're gonna be using fluoroscopy. And they found that the median effective dose, depending on what procedure you're gonna be performing, is anywhere from 3.2 to 16 millisieverts. Keep in mind that the background radiation exposure is one to 2.3. So it's anywhere from three to 16 fold higher. So the good news is that the dose of the patient is not equivalent to the dose of the fetus. And that is based upon modeled projection radiation doses in patients undergoing SVT ablation. So one study looked at this in 20 women undergoing SVT ablation. They had 40 minutes of fluoroscopy exposure. But the average estimated dose of the fetus was less than one milligrade, which is equivalent to less than one millisievert for X-ray. But what is the threshold? Is one milligrade too much? Well, when it comes to cancer risk, anything less than 50 milligrade is not associated with an increased cancer risk over the duration of the pregnancy. But still, of course, less is more. And so it's also important beyond the radiation risk to look at what about the patients undergoing procedures? What about the other risks, such as hemodynamics, et cetera, and how do people do in outcomes? Well, again, we're going to case series and case reports. And one center reports their outcomes in nine women undergoing SVT ablation for refractory SVT management. And the mean fluoroscopy in this study was significantly lower than that noted in the prior study. It was 42 seconds, with some of those patients having zero fluoroscopy procedures. There were no adverse events in over the three to four year follow-up in either the patient or the mother. So when it comes to what the guidelines or the consensus document recommends, really the priorities are let's minimize radiation as much as possible, if not eliminate it, and let's also control the arrhythmia, because as we know, arrhythmias are associated with poor outcomes in the setting of pregnancy. So when it comes to recurrent SVT, that is drug refractory and or unstable typical flutter, or certain types of VTs, the recommendation is a class IIa, such that catheter ablation is reasonable. But I'm highlighting here the fluoroscopy use and lack thereof. And then when it comes to recurrent atypical flutter or atrial fibrillation and consideration of ablation, now we're in more of a IIb recommendation, so something that can be considered after a shared decision-making process and seeing really what is best for the patient. Timing is important. So once you decide with your patient, let's, okay, we're gonna do this, we're gonna undergo an ablation, do an EP study, when in the pregnancy is important as well. And as, again, the other speakers have alluded to, this is a theme, right, as pregnancy goes on, the diameter, volume, area of the IVC goes down in the supine position. So of course there are considerations when it comes to what happens when you're gonna have a patient who's supine under general anesthesia, or any anesthesia. So if the procedure is done later in pregnancy, it is recommended that the patient be placed in a left lateral tilt position. And this is based upon the MRI data that Dr. Hoglar showed earlier. And it's because when you put that patient in that left lateral position, the IVC volume significantly is increased compared to other positions. So let's go back to our patient. So after a shared decision-making process, she did not want to be on medications. And I got input from her OB team, and anesthesia team, and her referring cardiologist. We decided to go ahead and pursue ablation at 22 weeks. I did not want to perform a procedure in a left lateral tilt position. And so we did this without thoroscopy. We also used intracardiac ultrasound. And so this is what we saw on the way up. Little high, little hand, and then the heart. All right, so we used something called open window mapping. And if, you know, for those of you who do a lot of accessory pathway ablations, I love this. So this was, it can see, oh, this was actually manifest, but I can only induce ORT. And so I mapped both the V and the A insertion. And I mapped the V insertion using open window mapping, and you can see where the signal crosses the tricuspid annulus, this is a posterior septal pathway. And then also then mapping the A insertion during tachycardia. And this was a successful site of ablation. And so fortunately, she's had no anterior, or no accessory pathway reconnection or conduction, and she subsequently delivered a healthy baby at term. All right, so going to R, what isn't the best thing to do? So it really is not waiting to do anything. So this was a high-risk patient, a patient who is having syncope, palpitations, and the setting of WPW. So we could have done medications, of course, but, you know, after our decision-making process, we decided to go through with the ablation. So one more part, device implantation. So this is a 25-year-old woman who was 19 weeks pregnant when she suffered an out-of-hospital cardiac arrest. Fortunately, she made a complete neurologic recovery. No reversible etiologies were found. She was also quite bradycardic. So what are the best next steps? So do we go ahead and implant a dual-chamber ICD with methods to reduce fluoroscopy use with multidisciplinary input? How about implanting a sub-QICD? Or do we just start amiodarone and perform the ICD placement if the VF recurs? So the National Inpatient Survey was utilized in a study looking at four-year outcomes in pregnancy-related hospitalizations and looking at the incidence of pacemaker implantation. It's not common, but it does happen. So pacemaker implantation in this four-year study, the incidence was 0.003%, and most of those patients underwent transvenous device implantation with some percentage undergoing leadless. And they found that those receiving pacemakers also had more comorbidities, which makes sense, and such that the unadjusted mortality rates were higher, but yet when adjusted for those comorbidities was just the same. So going on beyond mortality, what about outcomes and how do you perform the procedure? How do we do this? So electroanatomic mapping can be used for device implantation to minimize or eliminate radiation exposure. So case reports have shown the utilization of EAM, implanting either single or dual-chamber pacemakers, but the problem is with EAM alone, you can't really quite see the slack. You can somewhat estimate it, but you can't really see it. So another set of case series also showed adding ICE to this to be able to utilize or visualize the slack. With ICDs, there was one case report utilizing TEE to be able to visualize the slack and lead placement. And finally, there is a case report, at least one that I came across, of sub-QICD implantation during pregnancy. Of note, DFTs were deferred in all of those cases. So when it comes to what the 2023 expert consensus statement recommends, with placement of pacemaker placement, if it's irreversible and the patient is symptomatic, we put the pacemaker in with a goal to either eliminate or mitigate any sort of radiation exposure. And finally, it's the same for an ICD. If we have someone coming in with a high risk of recurrent sudden cardiac arrest, then we, again, need to minimize risk and put the device in. So let's go back to our patient. So we had a lot of input with what to do with this young woman. So after shared decision-making, we decided to go ahead and put in a dual-chamber ICD because of her significant bradycardia. And so we utilized electroanatomic mapping. And so we got ultrasound-guided access through the axillary vein, and then I put a decouple catheter in to create a fam shell of the SVC, RA, and RV. And then I hooked the leads up to the electroanatomic mapping system so that I could see the lead tips. And there I'm just pointing out, and it isn't my best map ever, but I also didn't want her to be on the table for too long either. So as long as I could see the tip, it was great. I did use a teeny little fluoroscopy, so I cheated just so I could see the slack. And so the fluorotype was 0.4 minutes. And here was her post-op day number one X-ray. Subsequently, it's delivered a healthy baby and no therapies thus far. So going back to the question, what are the best next steps? Well, you saw what I did. So I went ahead and implanted a dual-chamber ICD after lots of conversation in reducing her risk. So let's summarize real quick. So our goal for the past 10 minutes was to look at some of the data that we have and also how to perform invasive procedures in the setting of pregnancy. Cardioversion, it's safe, and you really just do it akin to what you would do for the non-pregnant patient. Ablation can be performed safely, especially if you don't use fluoroscopy. But the planning really should be multidisciplinary and pay attention to the timing during pregnancy. Device implantation, the same thing. Minimizing fluoroscopy as much as possible. Utilizing the tools that we have that we more often use for ablation, but they can be used for device implantation as well. That's all I have. I'm excited for the discussion. Thank you. All right, we have a few questions because we're getting close to the hour. I'm going to do a rapid-fire session, okay? We're going to have the speakers. I'm going to go to them. 10 seconds to answer the question. The first one. PBCs burden play a role in mortality of disease progression in pregnant woman. PBCs burden in pregnant woman the same as in non-pregnant state, meaning that high PBC burden could potentially cause heart failure in woman, and there have been some reports of worsening fetal outcomes if it's a high burden, like in adults, 10, 20% high burden. Fortunately, majority of women don't have that. Question for, do we have, Dr. Wright, do we have any data of cardioversions before 16 weeks? Are there any higher risk to the fetus? I don't expect that. What do you think? High risk for the fetus, cardioversion before 16 weeks? No, not that I know of. I think it's the same from what I know. I think it will be the same. I always expect very low risk. The fetus will be smaller, further away from the heart. Actually, I think the risk of cardioversion is overstated. You can't actually touch the patient when you're doing CPR, cardioversion. Nothing ever happens, promise you. I do it all the time. Tess, fetal dorsal de pointe, if you give him magnesium, do you need to put the patient in the ICU? Oh, that depends on your team and their comfort level where to put him, with the OB, ICU. I've done it in the ICU, but I've also done it in the OB unit, like in the delivery unit. Question here, would you consider the fibrillator vest or re-implanted ICD until delivery? The answer I'm gonna give it to you is no. The patient can get a device if it's indicated. ICD or pacemaker, the risk of fluoroscopy is very, very low. No kid will get a malignancy from the risk from radiation, from essentially no cardiovascular procedure. So the message you get from this panel today is you treat the pregnant patient as you would, according to the indications. If they need a ICD, transvenous, subcu, just do it, because the risk from radiation exposure is marginal. What else we have here? Arrhythmias, Tess, arrhythmias in the fetus. Does that mean that the fetus will have arrhythmias later in life? Great question. So flutter tends to go away. It's usually after birth, we cardiovert, and they don't come back. They don't come back. Unless they have a substrate, like an accessory pathway. Right, if they have SVTs, they tend to resolve by about a year of age in all kids, WPW and SVT, and about half may come back later in life. Dr. Wright, approach to, Tomolo, approach to sedation during pregnancy. Yeah. I always consult with our OB anesthesia team, usually at 22 weeks or so. They're thinking about doing more general anesthesia than sedation because of the risk of obstruction of their airway, or maybe a little bit more than 22 weeks, but that's where they start thinking about it. Question, Dr. Wright, PFA versus RF. I don't know of any case of PFA in pregnant woman. Do you know anything about that? No, not to my knowledge. What else we have here? I'm missing something. It's 4.30. How did we do? Baby X, after birth, had SVT and was treated successfully. So, I think we got to 4.30. How was that? Great, thanks everybody. Thank you so much to the audience for staying here with us, and thank you to the speakers. We have a bunch of rapid fire questions. Thank you so much. Enjoy the rest of your meeting. Thanks so much.

arrhythmias

pregnancy

cardiac complications

hemodynamics

beta-blockers

fetal arrhythmias

cardioversion

ablation

Brugada Syndrome

Long QT Syndrome