Dr. Div Patel discusses a patient case of neurocardiogenic syncope, the symptoms it produced, the evaluation and treatment plan initiated.
This is a short talk but I think uh new therapy, I think it's important to talk about these patients who suffer from neuro cardiac neurocardiogenic syncope. And so these are patients with vasovagal syncope who have recurrent issues uh with passing out. Um and then new therapies in this space. And it's important to note that I sort of learned this technique, which was nice. I learned it after fellowship, I learned it looking at papers, talking to other electrophysiologist and sometimes in other countries. So the main guy who started this technique started in Turkey, he's over in Turkey um and then learning talking to other electrophysiologist. So we'll start with a case. This is a early 20 year old male who presented to the er after witness syncope. So he states that prior to the episode, he started feeling lightheaded and dizzy and then everything went black. A similar episode happened about two weeks ago when the patient was walking out of the store and this is his second er visit. So he's presented multiple times with Syn, he in the er because his troponins are negative um and they call him a 20 year old, they say you're a low risk syncope, go home and he keeps presenting back and back from the, er, this is one of his rhythm strips and you could see, um, he has a P wave, a QR s then a P wave nonconducted QR s and he goes to 2 to 1 and then all of a sudden he has a V block, um, and it lasts about 7.2 seconds and the important part of this A V block is it's vaguely mediated. Do you want the sinus rate if the sinus rate is slowing before a V block, it indicates that it's vaguely mediated com compared to paroxysmal A V block that is concerning for his Perini disease. So here's our management options for this patient. He remember he's in his twenties, he's presented multiple times with vagal syncope. Uh The management options of vagal syncope include conservative management. So fluids, sodium compression stockings, you could do a leadless pacemaker implantation. Given his young age, you wanna avoid putting in hardware in the body, especially transvenous route because you know, long term lead management, the rates of fracture go up every year that he has the device, infection risk is there. Um you could do AC LS pacemaker. So Bron using RV impedances and mu muscle contractility has a specialized pacemaker to help these patients. But you know, he's in his twenties or you could do an evolving therapy which is neurocardiogenic cardiac catheter ablation. So, before we talk about which one of these we chose for him. I'll just talk briefly on syncope. So the definition of syncope by Webster's dictionary is fainting or passing out. Um And the most important part is the history and physical exam. And I tell all of the pas when we go down there, the two things that make me worry for rhythmic syncope is a lack of prodrome. So did you pass out and not feeling coming on and trauma? So any time they have trauma to face trauma, anywhere else, you know that this person had probably an arrhythmia that caused their syncope. Vasovagal syncope is more suggested by history. It usually occurs in younger patients. So patients in their twenties and thirties um and then they, they feel a prodrome coming on. So they feel nausea, vomiting coming on, they feel that period of blacking out coming on. And that's because the sinus rate is slowing their pr is prolonging and then they'll pass out. So, prodrome with some nausea, vomiting component, some G I component is consistent with vasovagal syncope and then the causes of syncope are important to think about. So, if we think about cardiac causes valvular abnormalities such as severe a stenosis arrhythmias, we saw a patient last week with VF and Brugada syndrome. Um so definitely can present like that orthostatic. We see especially in older patients, especially after a hot sunny day. They may be dehydrated. Um neurocardiogenic such as this patient presenting with vasovagal neurologic can present. So C va s and seizures and a lot of times patients with cardiac syncope will be mistaken for seizures and they'll get some kind of epilepsy monitoring to later find out that it was mostly cardiac which causes their syncope. We see dis autonomia. So I wanna make sure we separate neurocardiogenic from pots because I have no interest in caring for pots patients. I I applaud people who do uh but pots patients have dysautonomia which causes their heart rate to raise up. Um And then Parkinson's and diabetes because of the autonomic dysfunction, they also get pre syncope or syncope and then we have metabolic causes. So if you go to code or syncope, you wanna make sure their glucose is ok. Um And make sure they don't have any abnormalities in electrolytes or things like that. The tilt table test. So Doctor Robertson reads a lot of these. Um but a tilt table test, you don't really need it for vasovagal syncope to clarify. But in a tilt table test, you're basically measuring the blood pressure. You're looking at the EKG um as you go from a supine to upright position, back to a supine position and then you're just looking at both the heart rate and blood pressure at different rates. Um And you do these for patients to confirm pots or orthostatic or other kinds of syncope when you're unsure of the diagnosis. But in our case, the patient was in his twenties. He we knew that he felt it coming on. We saw pr prolongation um and sinus L consistent with vasovagal syncope. So here's some tilt responses. I think it's a good idea to know what tilt responses mean uh for different diagnoses of syncope. So this is a normal tilt response. So you go from a supine to an upright position, your heart rate s slowly increases your blood pressure basically stays the same. It's a normal response. On the right here, you see a patient with pots, they have a markedly elevated heart rate. As you go from a supine to upright position, the blood pressure dips slightly um but not a drastic dip in this patient with pots on the bottom left. You see a patient with orthostatic hypotension where the blood pressure as you go from supine to upright drops drastically. Just like when you're measuring orthostatic vital signs, the heart rate increases slightly. And then here you see, um the one that we want to talk about today, which is vasovagal syncope where they're doing. Ok. And all of a sudden, their heart rate drops, their blood pressure drops and they actually pass out and they should have ended the tilt before this happened where the heart rate went to the forties and the blood pressure went to zero. But that's beside the point. So these are the four common tilt responses you'll see um when looking at a tilt table test to discuss the anatomy of the vagal ence into the cardiac system. So it's important to know that vasovagal syncope. I tell patients it's not a cardiac abnormality, the heart is fine, it's more the eer fibers that lead into the heart. And so you can see ganglionic plex size. So this is an anatomical view and you could see there's small nerve fibers that basically cross at different areas of the heart. So this is located in the superior vena cava through the aorta, there's different fibers in the right superior pulmonary vein into the right atrium. There's IVC left atrium near the bottom of the heart. Um And so these different ganglionic plexi are what's supplying the vagal inputs into the heart. And so you can imagine a cool electrophysiologist was like, hey, if I get rid of these, maybe I'll be able to affect the vagus supply to the heart and be able to solve these arrhythmias. And so if you can imagine if you try because we're electrophysiologist, we don't like opening up the heart. We're like, if you deliver enough heat energy at these areas, just like in a fri population, you could target these fibers pretty, pretty readily. So that's an anatomical view if we go to electro anatomical anatomy. Um This is both of the right atrium and left atrium. This is a 3D map created by uh a mapping catheter. I think in this case, it was an HD grid. But you could see different spots here where the same anatomical portions correspond to this electro anatomical map. So here, same thing, this is where the sinus node originates aorta SVC junction um outside the left superior ganglionic plex sign, both the right atrium and the left atrium. On the right side of the picture have eer vagal fibers to the atria. And so if you target those with ablation, you could affect the vagal inputs. And there are electrogram corresponding to these ganglionic plexi. So on the bottom is a normal deflection. So when we're mapping, we see a single deflection, we see a high amplitude frequency indicating normal voltage of the atrium in these kind of areas where they have um ganglionic plexi. You do both. You look for um you look for fractionated electrogram, both low amplitude fractionated electrogram and high amplitude fractionated electrogram. And using both the knowledge of the anatomy of where the fibers sit as well as looking for these kind of signals with high fractionated electrogram, you can actually map these ganglionic plexi and then burn them away. And so that's what he did. Uh Initially the first kind of cases he did in Turkey, he used both anatomical and fractionated data to look where they insert and they basically insert in the same places up near right, superior pulmonary vein, right, inferior pulmonary vein, left, superior pulmonary vein, left inferior pulmo pulmonary vein. And using those knowledge of fractionated electrogram and an anatomy, you could target those with catheter based abortion. So I'm looking at Jeff because Jeff saw this patient in the er and so this is his consult note and Jeff writes the best attestations uh for his patients and the, and it was a thoughtful consult note. So his note says history and telemetry tracing are most suggestive vasovagal origin. True. Moreover, resting EKG also shows evidence of high resting vagal tone with sinus arrhythmia. The concerns for seizure, like I said, people sometimes confuse syncope for seizure during the episode. Our most reflective of hypoxic myoclonus nevertheless suggests neurology consult. Given family history of epilepsy, we discussed conservative measures which he rightfully. So he picked option a such as focus on hydration, somewhat increased salt intake and compression stockings. We also discussed that the condition is overall benign and often self limited and generally resolves with age. We will also get baseline echocardiogram and recommend extending monitoring upon discharge. Unfortunately, given the recurrent nature as the yet to completely explain etiology. Patient must forego driving for six months per Virginia law, uh which is the state law in Virginia. If you sync A P you, you can't drive for six months, which is why it's debilitating this kind of condition if these episodes were to continue. Despite conservative management, given the profound cardioinhibitory nature of the telemetry strip pacemaker may be warranted. We would likely we would obviously like to avoid that at all costs. Given his age. So this was the right approach. First time patient presents with vasovagal syncope, you try conservative measures, but now back to our patient, the syncope returned. So given classic and this is uh Doctor Harron Nee uh attest station, which she she rightfully wrote a detailed note and called me about this patient as I had done one other case for this for this condition. So she writes that given classic prom prior to the episode in telemetry, findings of sinus pauses, predominant neurocardiogenic syncope, he was advised of lifestyle changes. However, prior to discharge again, had syncope f despite following lifestyle modification yesterday, while in the car had a program then passed out again while in the er, he had another episode of a 15 seconds of sinus arrest. And so if you can imagine for the parents, the kid 15 seconds of aces where everyone's running in doing chest compressions, it's a debilitating condition. And so she rightfully wrote in her notes, it's a class two B guideline to put in pacemakers over the age of 40 we don't have great data on pacemakers under the age of 40. And so that's why it's a black box. What do you do for these patients because they're gonna have lifetime management of their device. Do you do a leadless pacemaker? Knowing that it won't provide the best a V synchrony? Do you do cardio? Do you do Ac Ls pacemaker or I talked to the patient and the family and I gave them four or five papers and I said I've done one case. This is, these are the type of things we're looking at is would you be willing to do a cardio neural ablation um to treat this and avoid long term device management? And so the family read all of their options. The patient was in, in his twenties and we decided to proceed with a cardio neural ablation. So here's the map. This is the anatomical map. This is the right atrium. So this is the SVC comes down here, this is the lateral, right atrium. And you can see IVC here and you could see we're targeting targets here located on the right atrial septum corresponding to the uh right superior pulmonary vein. Here's the P A view. So, posterior looking back view of the left atrium, the four pulmonary veins, this is the left superior, left inferior, right, superior, right inferior. And then this back here is the A P view. This is the mi annulus cut out, this is outside the right superior pulmonary veins and left superior pulmonary veins. So this is the right atrium, left atrium. And so these are full four pulmonary veins, 1234 we targeted here, we saw fractionated electrogram corresponding GPS right here outside the right uh right inferior pulmonary vein. That's an A P view, anterior posterior. So this is mi annulus and then outside the right superior and then left superior up there, we targeted those for ablation and this is electrogram before during and after the case. So initially, the patient showed up in sinus rhythm with a slow heart rate in the fifties. Um during ablation, we induced wanky bach and there was periods of 2 to 1. And then with ablation, we actually resolved that 2 to 1 and heart block um into a faster sinus rate. So the first one, as you could tell the sinus rates in the fifties, we start a blading and we cause wanky bach, it goes to 2 to 1 to almost complete heart block. And then with ablation, we see resolution, normal conduction and a speeding up of the sinus rate with the cycle length of the eight hundreds instead of 1000. So it's a nice response to see. You wanna see some A V block when you a blade and you want to see the sinus node pick up. So you want your average heart rate to pick up by 10 to 15. And that's just means you're, you're targeting and you're affecting those vagal inputs into the heart. So the end points of ablation in a patient with persistent A V block that you've caused, you should have some return of 1 to 1 A V conduction in patients with Permal A V block. You wanna have at least one of the following. You wanna have apr that shortened to 75% of the recorded um And if you give atropine, you want that to see that pr shorten um by at least 75%. So we put a, I think it's important when you do new techniques to put monitors because we want to make sure there are a lot of people who think a lot of eps placebo effect. And so you wanna put monitors just to prove to people that it's not placebo and just to make sure you don't see any A V block afterwards or you see a difference in response. So his monitor on the left is before his ablation. So his low heart rate was 43 high heart rate of 193. He's a young kid and patient was monitored for 21 days. Seven triggered events, pauses greater in two seconds occurred two times with the longest pause of 16 seconds. Um And so that was his pause and his monitor. Um and then afterwards, we had a minimum heart rate of 34. So he's able to dip down maximum heart rate of 190. So that heart rate variability stays about the same. But his average heart rate if you take a look is now 98. So it went from 75 to 98. And that, that's one of the things with these cardio neural ablations is their heart rate will raise and maybe they have an attack, but the ATAC doesn't cause them issues. They don't, I've, I've now ablated four of them, they don't have symptoms from the at attack. They have more profound symptoms with a V block or things like that. So even those average heart rate is 98. Now it doesn't bother him or affect him. Slight p wave morphology, changes were noted and that's probably different kinds of ectopic atrial rhythms taking over, but there's no evidence of pauses. Um no evidence of a V block. There was one incidence of winky bach when he was asleep. So basically, we increased the average heart rate. We've resolved the A V block in this patient. Um And the patient did well. And so I say the proof is in the pudding. Uh The patient followed up with neurology because he also had this weird episode of uh maybe a seizure. So this is the neurologist assessment. This is him seeing him eight months later. Uh The patient is a pleasant 20 something year old who started passing out in May of last year. Reportedly, he had an episode of convulsive syncope in June. He was diagnosed with cardioinhibitory predominant neurocardiogenic syncope underwent ablation. Fortunately, he has no further syncopal or pre syncopal episodes. And so the neurologist said no further recommendations continue to follow up with cardiology. And so this is nine months down the line. The patients now able to go back to college without that impending fear of doom. They started driving again, which is a huge quality of life benefit for this patient I had another patient um who I ablated and the patient was on long term disability um with this kind of condition because they kept passing out at work and the work deemed them incompetent. So I got this message because we need people back at work. She, she actually wanted to go back and she said she sent this message saying uh thank you for performing my ablation. I was on long term disability for medical issue that's now been corrected and she's back to working as a full time teacher. And so these are the kinds of patients you're seeing younger patients with this kind of condition where it's definitely affecting their quality of life. So just to briefly touch upon a couple of studies because this is such new technology and new type of treatment. This is a paper published uh by in Europe looking at both non pharmacologic treatments and cardio neural ablations in patients with vasovagal syncope. So they took 48 patients with symptomatic recurrent reflex asystole um which is what our patient had. So the importance of this is recurrent. And so doctor Hadley's idea of the first time saying fluids, compression, stockings and and salt. It's the right idea if it's your first time. But now what if you have two episodes, three episodes, four episodes. And so these are patients who had more than one episode, they were randomized to either cardio neural ablation or non pharmacologic treatment options. Um And you and those are the ones he mentioned. So fluid so compression stockings avoiding triggers and you could see the Kaplan Meyers separate right away and stay separated for a long period of time. So you could see in the blue in the cardio neural ablation, they had no no real syncope, syncopal episodes at 24 months of follow up, the control group right away, started having episodes and you could see a wide separation, the quality of life before treatments were the same in both groups. And you could see on the bottom that the quality of life was significantly better in the ablation arm compared to control group, which stayed the same. And so I think we have some emerging data that at 2 to 3 years, these patients continue to do well um live without recurrent syncope. What about pacing versus ablation? So I talked about the other options of CLS pacing or leadless pacemaker. Sort of depends on your values, your long term risk of having hardware in the body and whether you're up for an ablation procedure, which has some risk uh versus having a pacemaker, which has more long term risk compared to a procedural risk. So you can see here, the Kaplan Myers are pretty similar ablation takes a little bit longer than putting a pacemaker in uh for procedural time. Adverse events are basically the same uh pacemaker patients had effusions, some pneumothoraces, uh cardio neural ablation. There was one incidence of effusion that was tapped otherwise um minor, they called it ectopic atrial tachycardia, which was asymptomatic in the majority of patients. But you can see that Kaplan Myers no significant difference um in syncope or symptoms in follow up after adjusting for baseline characteristics in both groups. So I think the approach to patients with vasovagal syncope has to be individualized depending on age discussion with the patient discussing with the medical provider. So this is a nice flow graph. Um coming from a paper discussing cardio neural ablation versus pacing. And it talks about that in younger patients, we should consider cardio neural ablation first. So in patients younger than 40 who want, you wanna avoid long term risks with device management, you should probably do cardio neural ablation first in patients who are older than 60 where that device, you know the battery life. Now last 10, 7 to 10 years, they're not gonna live past 90 or 100. You may wanna consider putting in a pacemaker first and then there's a gray area just like anything else where if they're between 4060 you do an individualized approach and you could do either or if one of the treatments fails. And that's what I told this patient if you're in your twenties and if our ablations fail, we could just put in a pacemaker uh down the line in a month or two. All right. So just to wrap up about this um syncope evaluation requires a careful history and physical exam. Conservative therapy is the first option in pa patients with vasovagal syncope. Um and then in patients with recurrent vasovagal syncope, neuro cardiac ablation may be an option to improve quality of life. Long term results on efficacy are unknown but seem to be as efficacious as pacemaker implantation and improves quality of life. And then future studies are needed to examine hard end points of when to stop ablating. Because uh if you give an electrophysiologist, an ablation catheter, they'll keep ablating and which patients will benefit the greatest. And so I just wanted to say thanks to the rest of the EP team.
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