 Thank you for the kind introduction. So before we start, I just want to kind of go through the disclosures here. I'm what I'm going to be presenting are a series of ideas that we have come up with and we have developed over the course of the past few years. To be clear, none of these at this point have been clinically cleared. Some are very close and on the precipice but at this point nothing is cleared for human clinical use and here are my disclosures. So I'm going to present a series of problems that over the course of the years we have all faced and I can guarantee you that every physician in this room has dealt with every single one of these problems except maybe one of them. To make the point that as doctors, at least the clinicians in this audience, that you have a unique opportunity that if you kind of take some time and try to think a little bit outside the box that you alone really can understand what is needed in the heat of the moment. Then you create a network and here at Texas Heart and at St. Luke's you have a very, very unique opportunity to integrate your clinical knowledge with the engineering expertise with all the other resources that are basically you're embedded in. So I would advise that you take this opportunity very seriously and make the most of it. So having said that the way I'm going to proceed is I'll start with some clinical problems and again the solutions and what we've done with them. So I was advised to use the computer scroller so we'll do that. So I'm sure everyone here who has done any type of a procedure has had to deal with the hematoma, growing hematoma, access site hematoma, or a bleed or even worse potentially a retroperitoneal hematoma because of my field of work in electrophysiology that's much less of an issue but especially with some of these newer technologies with mechanical support with the aortic valves and the triple A repairs that continues to be something that bedevils everyone. Here's a kind of a literature review of the incidents of vascular access site complications and I'll tell you a couple of things. In addition to this slide being a little bit confusing it's also a little bit old. So with those provisions in mind if you look at some of the major and earlier studies done looking at the incidents of complications the area of the circle represents the number of patients in the studies and the height on the Y axis represents the incidence of complications and so you can see you're ranging anywhere from 7% in the case of STEMI's to 29% and typically for them PELAS and typically the classic definition to make this threshold cut is any clinically significant bleeding but in turn in addition to that a 3 gram drop on your hemoglobin level immediately pre versus post-bleat. This is a problem that continues to be an issue and you know recently we looked at about 14 million discharges in the CMS data between 2012-2013 and identified about 37,000 target procedures. So again those target procedures were everything that you just saw except for the STEMI's. So mechanical support also no balloon pumps. So mechanical support with impellers or ECMO, the tavers and the triple A vascular repairs. So those 37,000 target procedures about close to 9,000 had what was defined as a bleeding complication and a bleeding complication was actually a pretty rigorous definition. They had to either be taken back for a repair they either had to or most likely and most commonly they had to have a transfusion. A drop in a hemoglobin was not part of the defining features of vascular access complication. So the majority of these patients vast majority actually ended up getting transfused. So the threshold again it's a pretty high bar. Those patients who bled had a 40% increase in the mortality rate. They stayed in the hospital longer and the cost of the system was significantly higher. Of these patients again as I said a significant percentage actually required transfusion by definition. So 20% of these patients actually ended up with transfusions and there was a clear correlation between the number of transfusions and their outcome. But that's for another day. So again though if you bled you were the bleeding either kills you or it maims you. You stay in the hospital longer and in addition to doing all that it really provides a significant increase increment in the cost to the to the system. Again this is in this cohort that was looked at and again the weakness of this study is that it was 2012 to 2013 and I recognize that much has changed. But again when you're dealing with CMS data there is a certain lag that is going to be unavoidable. And so you know this is a problem that probably significantly less than a few years ago but it continues to bedevil all of us even in the field of electrophysiology and the thought is is there a way that we can detect this early. And you know I had a situation about seven years ago. I was I had just finished a case here and most of you may know I you know every third week I go to Webster and Clear Lake area and so I finished a case here. I was on I-45. I get a phone call that you know one of my patients is not doing well and actually it was probably even longer. It was probably about eight years ago. At that point we were still doing lovenox and lovenox was really really bad when it came to the incidence of bleeding. He had a really high risk even with us in the venous system of growing complications and hematomas. And so the patient is hypotensive and I'm thinking to myself God I wish there was a way I could kind of interrogate that area. And for some reason I was thinking about some other feature of the ablation looking at impedances and I don't know it just at a moment the thought came we'll if we could actually interrogate the impedance of the site where the you know vascular access is occurring could we at that point say would there be a difference and my thought was that there would be because you know blood has very low impedance very low resistance to electrical conduction. Muscle I would think still pretty low but probably a little bit more and then fat and bone and all those other things you know definitely much higher resistance to conduction. So if you could put electrodes on the outer surface of these sheets and then during the entire procedure you could emit a sub physiologic and by sub physiologic I mean a sub threshold so it doesn't capture the nerve or the muscle. Could a change in that if there's a sudden bleed could that be manifested in the change in the impedance. And so here's basically a scheme of that where you know again this is very introductory for everyone here but we start with a simple you know vascular access sheath placement and you know most of the patients are half calcific disease or or other types of comorbidities that increase the risk of having a bleed it doesn't necessarily need to be a posterior so it can be a trauma just from the mechanical manipulation of the artery. And the problem of course that we have typically is if it's an anterior bleed no big deal you know you put some pressure you can see it and everything is fine. The problem is if it goes back into this via the hunter's canal into the gutter and I'm going to show you what this concept was. And this is basically a rendition of having the sheath same sheath except for the four electrodes. The four electrodes are emitting this electrical current and they're connected to the hub of the sheath and the hub of that sheath in real time is analyzing the impedance. So once you put the sheath in the analysis starts it gives you say a green light it starts flickering the electrical impedance is shown here and let me just stop it here and this field then is being interrogated by the by the impedance it's actually this is a little bit incorrect actually just like a magnet if you have the north pole and the south pole of the magnet the magnets field vector field isn't like this it actually extends beyond the distal tip of the sheath in this case about five centimeters and why is that important because distal to this typically is into the hunter's canal and if you have bleeding or cumulation of fluid into the retro spare peritoneal space and that's the key feature that will allow you to detect the cumulation fluid as you'll see in a second very precisely soon as any blood is introduced into into space as I said within five centimeters distal to this to the tip so having said that one of the concerns was you know look you have a sheath in place and most bleeding actually doesn't occur when you have the sheath in place most bleeding occurs after you pull the sheath because if there's a bleed there may be a tiny leak but the sheath often is tamponading the artery and once you pull the artery the sheet from the artery you know an hour or two hours later you may have a precipitous blood draw hemoglobin drop or blood pressure drop and that's when you have trouble and by the by then you don't have a sheath to measure that and I think this is a very very real and legitimate concern so the the way that you know kind of we've decided to frame this and I think this is something that has been kind of not accepted but has been the interventionalists have been more enthusiastic about than actually having a sheath that once you take it out you lose all measurements is you take that same sheath and you go into the vein right next to it and in this case you can do it even with a five-friend sheet because many of these procedures from my understanding they do actually have patients who have a venous sheath they're either to measure pressures or have a temporary wire and what have you and in this situation what you can do is you have that the sheath with the electrodes is actually in the vein right next to it now as you pull the arterial sheath back and the bleed starts accumulating the impedance starts dropping drastically and at that point you have that monitoring to be able to pick it up at the moment it's happening and not only to pick up the onset but to pick up the propagation and extent of bleeding and I'll let this finish just one more time here's the venous sheath arterial sheath arterial sheath is removed you have a little bit of a leak here once you pull out the arterial sheath the bleed blood starts accumulating and this venous sheath basically starts picking up initially one level of an impedance change then a second and a third and these numbers are not are not arbitrary in a study that was done to as and was ultimately submitted to the FDA about a month ago per the FDA specific request 20 animals were studied and in that study what was done is the controlled amount of blood a fresh blood was introduced into the perivascular space so that way there was control knowing exactly how much blood has been introduced and what the timeframe is and after about you know initial just to check the specificity of the system once the sheath was inserted a lot of torquing and torsion and moving around and all kinds of stuff mechanical stressors were applied to the sheath and you know the algorithm pretty clearly could pick up what was the real deal and what wasn't at the moment of bleed infusion and bleed infusion was 10 cc's per minute so you know it's it's not it's it's a leak maybe a robust leak but a leak nonetheless it's not a gusher the the device picked up every time that there was a drop in the impedance and there was a clear correlation then not only between the onset of bleed and thus alerting you that you have a bleed but also with the progression of the bleed which were defined as each of these lights and so this now provides a clinician with the potential to say number one I'm I have a leak I can do something about it I can not do something about it knowing that until that second light goes off in all probability we're looking at about 100 150 cc's of blood but probably not more once that second light goes off now you know you're a little bit more serious and you're going anywhere between 150 to about 250 and if that third light goes off you almost certainly have are dealing with more than 250 cc's of blood in that in that peri vascular space and so the correlation not only with the onset but with the progression so that's the first kind of problem again I'm sure every one of you in this room have had to deal with that just you know think about it try to you know try to not be hampered by what you have been taught in med school and in residency and I think that the best ideas you're in a phase in your training that you really are your mind is still open and you can come up with these solutions that I think can make a huge difference again this I will admit is not something that I deal with thankfully on a daily basis but the same component concept of impedance can be extended to other fluid accumulations in other spaces and again this audience is much more facile with the concept of indoleaks is a complication long-term complication of aortic graft repairs and and by extension of what I just said you know if you if the concern with an indoleak is that there's now going to be a communication that potentially will allow the introduction of blood or fresh blood into a space that up to now has been excluded and now has either clot or whatever have you but has been excluded from from the presence of fresh blood what impedances again be altered and well how would you check the impedance the most important thing I can tell you in this is location you have to be as close as possible that's where you get the most accurate readings and for a while we you know we were thinking go subcutaneous punch it in through you know behind their back or do something like that and then you know I remember you know putting up catheters in the EP lab and this happens to every one of us attendings fourth year second years when they put up those catheters and invariably as you're going up the right side you think you're going up and suddenly you know the catheter just buckles and you're like you know I wasn't there so you back it down and then you go back up and you try a couple of times and we keep saying torque this way and torque that way until you go into the main branch of the IVC and you go up well what is it that you're going in in those dead ends there's you know there's a lot of veins that I refer to as the inominate veins in the lower extremity but the IVC is sitting right next to the aorta especially at the abdominal limb and provides an excellent location these branches provide an excellent location they literally are hugging the aorta and so if you could put a catheter in there just like we do in the venous system it's going to be a dead end if you could again in the case of these veins I'm not talking about the IVC itself if you could embed it there then what would happen when you introduce blood into the area surrounding the aorta and that's what we did and as you can see and this I'll present the data in a second soon as blood is starting to be introduced into this area you see as expected an impedance drop and the challenge of this study is the mechanism in the model for having an endolyte that's a very tough model to create and you know I admit that this is this was not the prettiest model I just basically took a transeptal needle went up the aorta retro aortic access at the level of you know the abdominal aorta and with the transeptal needle it just started you know puncturing and and it wasn't that bad you know everything was fine and so then the impedance soon as you have that accumulation of blood which you can document just with a little puff of contrast the impedance drops and it dropped significantly and then after a while it tapered off and I think the aorta had sealed itself but again this was only one study we have not pursued this and this is the other I think the other motif you win some you lose some and you'll probably lose some more much more than you win but the chase is the fun part coming up with the idea testing it seeing that it works that you're not crazy and it gives you a level of confidence to you know the confidence to not be afraid to fail to fall on your backside and and so you know my backside's pretty resilient so it's I think it's really really important to to not be afraid of going for an idea that may not have been thought about before it's it's not because it's crazy it's just because you were the first one to think of it so I'll just kind of go through this a little bit more quickly so next is the concept of myocardial conduction disease myocardial dysfunction and ventricular arrhythmias so the reason that patients with the most common cause of ventricular arrhythmias in the post-infarct setting is re-entrant ventricular arrhythmias and what that is basically is anytime patients have heart attacks or for any other reason they have scar tissue what happens is the reason that they are predisposed to ventricular arrhythmias is because of delay in the electrical conduction and heterogeneity in the delay of electrical conduction in the heart now this is often through almost always through scar patchy scar in the case of non- ischemic cardiomyopathies and in case of ischemic cardiomyopathies more dense scar but it's an area really more so than scar it's in homogeneity of conduction that's the problem if everything was delayed together everything would be fine so if you look here you can see you know a conductive medium you have an area where there's a wave front you have an area where it's still refractory it's still resting and normally what you would get you know one wave would come then the second wave comes and everything is fine now if you create a situation where there is a little bit of a delay where there is and there's an inhomogeneity in that delay in other words if everything here was delayed equally this line would just move over here right and everything would be even but if there's inhomogeneity in the delay in other words there's an area that moves a little bit faster but there's an area that is just not able to keep up what that does is this area this medium that is excitable starts moving forward as it starts moving forward this area is still lagging behind so there's nothing to tell there's no rule that says you can't infringe on this tissue on this lower tissue from above so it actually starts moving forward and then it starts turning around you start turning around this wave front and as you start turning around this delay serves as an anchor and you have the initiation of a re-entrant beat a re-entrant basically a circle chasing ahead chasing its tail and in that situation you go from a normal rhythm to organized re-entry which we call ventricular tachycardia now when this wave when this re-entrant brick when this re-entrant wave front breaks down because again of those same inhomogeneities heterogeneities because of microscopic scar or what have you again smaller areas of delay here you know the water is coming you're standing in the pool you're the scar the wave front hits you you have little eddy currents form around your waist and now those eddy currents those little areas of wave block create newer eddy currents and those eddy currents cause what we call fibrillation chaos in the ventricle so you go from normal rhythm to ventricular tachycardia to ventricular fibrillation but the problem the crux of the problem is here the crux of the problem is the delay in ventricular depolarization that occurs again because of scar be it patchy non ischemic or denser scar so think about what is it that we do the drugs that we give amiodarone what does amiodarone do the conduction velocity it delays it what does Fleck and I do the conduction velocity it delays it what does so long due to conduction velocity doesn't delay it as much but still delays it is there any antiarhythmic that improves conduction velocity soon there will be you'll have these medicines that will be able to open the connection of the gap junctions the connects and 43 gap junctions but for now there isn't so this is why antiarhythmics can actually be profoundly pro-arhythmic by worsening this delay you actually can cause more more disease processes more arithmias and that's why some antiarhythmias are actually contraindicated in patients with myocardial infarctions what you want to do is you want to improve this conduction velocity and as far as we know right now there's no technology that does that to treat the underlying pathophysiologic mechanism of the number one cause of sudden death in this country and so with that thought and that background the the concept that we had and this was working with metopas quality at Rice University and Mark McCauley is intimately involved he's now at University of Illinois also our team with Brian Greene Matthews and and David Berkland and on and gonna put the I don't know they're they're all around here and and you know what the concept was let's take some conductive nanofibers and I won't get into the details of that but just suffice to say that conductive nanofibers think of them as thread-like physical properties with conductive properties of metal so they don't they're flex fatigue they're essentially resistant they won't fracture like metals will they have a contact impedance that is to say resistance to conduction and the ability to pick up current from tissue that's probably about about 10 times better than that of platinum or radio and so they have this remarkable ability to collect current conduct it and then dump it on the other end and so in this situation what you have is you start pacing this is the left ventricle of an animal you start pacing you have four decapolar electrodes sutured on the outer surface of the left ventricle and you look at the conduction velocities you start pacing here and you look at the conduction time from pacing in the middle here to each of these electrodes and for our purposes we're going to focus on these electrodes and at baseline before anything is done you see that okay everything is kind of you pace and you immediately capture it which makes sense because these are relatively close then you say okay I'm gonna make a deep lesion a deep RF lesion scar tissue in the shape of a horseshoe and I'm gonna keep pacing and I'm gonna see what does the conduction velocity do turns out the conduction velocity goes from about 26 it increases significantly as these things go again that's to be expected so then you say alright let me suture these fibers around this anchored scarf what then happens and you look again at the electrodes here and I'm going to show you what the other electrodes do in the next slide but when you start pacing again from here now with the fibers in position and looking at the electrodes that immediately oppose on the outer surface on the external surface of the scar these fibers and just again to be clear there is no direct contact between these fibers and the electrodes nor is there any direct contact with the pacing electrode what you see is that the conduction is pulled in the conduction velocity is reconstituted well maybe this is because of some mechanical feature you know you're thrown sutures and you're just approximating things turns out when you put a silk suture through as a control a non-conductive silk suture you don't see that phenomena the conduction velocities remain down and here's a video of that same here's the pacing electrode so you can see the good distance you can see there's a good distance here and here's the there's the horseshoe and you have the sutures so and the other point is if you it's only those electrodes remember four five six that were on the opposite side of those fibers that actually had them with the fibers had the normalization the reconstitution of that delay back to close to baseline again another feature suggesting that it is those fibers but probably the strongest feature that we have got to do tracing guys I'm sorry I can't give a talk without some intracardiac electrograms here but probably one of the most powerful suggestions for in a conduction over these fibers is if you put a catheter in the coronary sinus and the distal electrodes are labeled la1 and the proximal electrodes are five and so you have the lateral wall of the LV in the LA you have the septum and you're pacing from the ventricle so far so good so when you pace you're activating here and I'll tell you at baseline there was when you paste the ventricle at baseline there was no conduction so I'm gonna give you that right now and we're gonna show that in a second when you pace you notice on the coronary sinus catheters the coronary sinus catheter will pick up two signals it because it's hugging the left atrium and the left ventricle you will see the larger left ventricular signals and the smaller left atrial signals that's more magnified here the larger left ventricular signals and the smaller left atrial signals the reason that these are getting bigger is as you go distal the coronary sinus tends to hug more ventricular so as you are more proximal your relative size of the atrial to ventricular signal increases so the ventricular signal is going to be smaller relative to going more distal so you're pacing the ventricle everyone clear with this the big signals the ventricle you have activation and then you see for every ventricle here this is all this is time here and this is again location so a big signal a little signal big signal a little signal so VA VA VA but there's something else that you notice what is the earliest a you can see that the a here the atrial signal here is more separated than the atrial signal here but what's happening is that the impulse is coming up wrapping across this lateral aspect around LA one going to LA two then to LA three LA four and LA five and this happens with every beat at 480 milliseconds pacing one to one from the ventricle up to the atrium over this area where you had the fiber sutured now you remove the fiber and what happens you're still pacing the ventricle at 480 milliseconds so here's the ventricle remember the big signals V V V V what happens to these smaller atrial signals really there's no relation if you were looking at this if this was the a and this was the V you would say this is complete heart block and indeed it is except it's ventricular atrial heart block and soon as you remove the fiber that happens and so this is about as definitive as you know evidence as you can have that that conduction was indeed going up the fibers now I will also have to take a step back and say reproducing this in a sensed environment has been more challenging in larger animals in other words it seems at this point that in the larger animals we need for some reason to have a paced impulse to drive that current across in the smaller animals in rodents what we've seen that during normal rhythm spontaneously you will see that you can call it pre-excitation or that conduction from the atrium to the ventricle so there is a source sink mismatch issue that we need to work on so that the eight and during sinus rhythm and without pacing you have that conduction occurring to and so that's something that is a challenge at this point but we're working towards a solution I'm gonna do two more very quickly and then spend a couple minutes on the last one so pericardial access again most of you have been in those procedures we dread pericardial access unless you're dr. Rasek who seems to have an unusual interest and enjoyment with them and and so what you know what the dread is of course is that needle when you're trying to get access that can go anywhere you know that it's happening even in the liver we all read about stuff that happened goes into the lungs you know you put a wire and you think you're in the RV you put a in the pericardium you put a sheath in and you know you just poked a hole in the body of the right ventricle so again across the this is my last impedance based moment or impedance based concept but could there be that same needle that you use could there be a signature impedance that could help you differentiate between the anterior mediastinum the pericardial space and the right ventricle and the answer is yes that there is a clear difference in near field impedance between the anterior mediastinum you go under the under the sternum that's that tissue the diaphragm things of that nature and you start pushing in and versus the mediastinum itself versus the right ventricle very clear demarcations and I always say that I'm I get a little embarrassed to show this ROC curve but this is at least the data that we had this is the way that analysis look so with this data in mind with at least the so this was a catheter that we placed and we would go into different spaces and looking at the near field impedances this was not the needle itself so but with this knowledge now we said okay let's see if we can take a needle put embed electrodes this is a regular old you know 18 gauge needle embed electrodes on the distal tip and make sure those electrodes again you have to have they have to be insulated from each other because the relative impedance delta that you're looking at is between these electrodes okay so we have these electrodes here we have the wiring in the body of the needle and then that but this wiring is connected to our impedance meter for lack of a better term and so I bet you guys can tell who this is and also who this is but so downstairs we said okay let's do it let's go advance the needle just like you would fluoroscopically with the same guidance and everything else and let's see what happens and here is Dr. Berkland and you can see that he's positioning there's a sternum he's going sub-ernal and he's I don't think you're going to see the advancing of the needle I doubt it yeah so he's advancing it but so this is this is what you do every day now every time that you're trying to get a dry tap this is this is a technique that should be familiar to everyone and what and what you see is that there is a dip this is the raw data that at the anterior metastinal space as your again impedance is on the y-axis this is on the time is on the x-axis as you transition from the anterior metastinal space to the pericardial space you have a drop in the impedance again it's reproducible we've done two studies so far and it's multiple attempts at each and it's very very clear cut and so the concept then is so in this case what we did is we introduced it Dr. Berkland then went and what we noticed is the diaphragm actually causes a drop in the impedance too when you go through the diaphragm that's the first drop in impedance that you see and why because it's muscle muscle has blood muscle has tissue so you would expect that that tissue versus the fat and the bone of the anterior metastinum would have a lower impedance and indeed that's what you find so this is Dr. Berkland on purpose going back into the anterior metastinum so anterior metastinum or it shouldn't be it's still in and right behind the sternal entrance the diaphragm again back diaphragm back diaphragm back now he decides to go all the way he goes through the diaphragm into the anterior metastinal space and soon as he goes in to the pericardial space and he confirms it by contrast the impedance drops again and so you now have a means of that needle tip actually telling you where you where you are of course it requires a lot of a lot more work but at least the initial data looks looks pretty promising two more things and then we'll be done here the dreaded esophageal fistula complication so many of you who've done the ep rotation are familiar with this scary and unpleasant situation in the lab here you have a three-dimensional map of the pulmonary veins you're actually looking at the left atrium from the back so a posterior view of the left atrium the pulmonary vein this is the right inferior pulmonary vein just looking at it from slightly different angles and so we're looking at the back going in and how we create this map don't worry about it there's catheter there's catheter that we use that looks at voltage creates a gps-based rendition in 3d and so you create a voltage electro anatomic map of the left atrium and this is a spiral catheter it's got 20 pulls on it we call it a lasso that goes at the opening at the osse of the pulmonary vein so this is right now kissing right at that tip of that pulmonary vein and you know the the thing that you can appreciate is is really this is fine what's the problem well this catheter is in the esophagus so this is a catheter that is hugging a temperature probe it's again a mapping catheter and this allows us to localize and since it's hugging the temperature probe by taping it to it you see where the temperature what the temperature is but also where the location of the esophagus is and i did this because i wanted to make the point that this isn't just one view when you rotate you can see that this esophagus is right on the pulmonary vein and by frame of reference this distance is five millimeters so you are very close to the esophagus and why is that a problem well one of the biggest well not the biggest but the most dreaded complication of aphiboblation is atrial esophageal fistulas the mortality approaches 80 percent it is a devastating complication patients die and they die a terrible death and really for a procedure that at its core remains even you know in the worst of situations a semi elective procedure and so you know what was the solution in that case i had to use cryo because and even cryo has been reported to have atrial esophageal fistulas but certainly a fraction if that of what you would see with with rf application so this is the cryo pro balloon setup so so the thought was is there a way to move the esophagus away and that's not anything that's new people have thought about it they looked into it you know you you take a stylet and you try to push it one way or another the studies that have done that though when they've looked endoscopically they've actually seen an increased incidence of ulcerations and the thought is that probably just the mechanical trauma of trying to push the esophagus in one direction so you have a leading edge and you're pushing against that leading edge that trauma may be as worse as anything else the other problem is you have a leading edge but what about your trailing edge are you moving the entire esophagus you know along and so some studies have shown that you can do that um but the thought i had is is there a more a traumatic way of doing this in the thought that we and why not try to suck the esophagus does that make even sense is the esophagus well the the reason that i kind of we thought about this was in the beginning we used to give contrast to these patients oral contrast back in the day where not everyone was under general anesthesia you would have them swallow a little bit of contrast you would see that bolus of contrast and you really would see the esophagus is a pretty dilated uh organ now and then you'd have a peristaltic wave front and it was such that sometimes i would wait to time my ablation around a vein waiting for that peristaltic wave front to come because when it would come the esophagus would contract and as it's contracting it would go away from the vein that i was trying to blade around so you're waiting there you know peristalsis comes let's burn let's burn then the next peristalsis comes so why not try to do a suction and so suction straightforward again you have a regular temperature probe it's got some fenestrations some openings in this plastic tube there's a balloon distal a balloon proximal and when you're in the esophagus you're ablating you're doing your thing the balloon is down everything is everything is fine but now let's say you're getting close to ablating say this vein in that case all you need to do and you want that peristalsis you know you want to have that contraction all you do is you open up this balloon on either side and you apply suction this is an open chest demonstration here's the esophagus again we're not inflating and deflating this is the baseline size of the suffix i gotta be real clear about that when you when we put when you introduce to the box it's it's a low profile so the esophagus is not you know you're not pushing away the esophagus the balloons are on one end and another end and then when you apply the suction you can see that this dilation comes it kind of sucks it in and so it's a very straightforward you know nothing and then you have the temperature probes on it too so here are the fenestrations balloon distal balloon proximal what does this you look under x-ray this is what it looks like you're applying the suction and it basically creates that peristalsis but the esophagus kind of collapsing now clear cut limitation if my pulmonary vein is right on the middle of this esophagus the collapsing it is not going to do anything i mean that is that's for sure but you know it it's it's still pretty nice to know that you can decrease the the caliber of the esophagus by you know something like 80 or so because in those situations every millimeter really does matter you may say well who cares it's you know the incidence is one in 2000 it's the same thing what is the incidence of retroperitoneal bleeds and guess what this is much more lethal than any retroperitoneal bleed what it does is it makes the ablations longer the success rates probably a little bit lower it makes gives me a lot of gray hairs and frankly you know it's something that is a major obstacle that we have to deal with pretty much in 50 60 70 percent of procedures so the reason that you're not we're not seeing the complication rate is because we are spending so much time dealing with it to prevent it in the lab and that's the that's the issue and so now i'm gonna end spend a few minutes on the concept of defibrillation so just to be clear this this pacing based defibrillation we have not in any studies done ventricular arrhythmias and cause pacing defibrillation i'm going to give you a little bit of background into what's going on and then kind of what the hope is to to go moving forward so defibrillators are you know we don't need to discuss those we all know what they do they shock and we know what their problems can be you know lead malfunctions lead fractures patients who have no vascular access etc etc and now there are actually leadless pacemakers one of them has actually been FDA approved the other one i expect that within a calendar year will be but suffice to say that those pacemakers now do not are leadless but at this time at least they're also a single chamber device that is quite large and and you know you use i think it's a 24 french venus sheath to to insert them again forget about the names but these are not small devices but more importantly with regards to the defibrillators the subcutaneous defibrillators have the opportunity and now commonly used with them you also avoid vascular access but in the case of the subcutaneous defibrillator you tunnel the leads under the skin here's the defibrillator can under the left uh castle region and you tunnel the leads you go across the breastbone across the sternum and the vector is the left ventricle so it's sandwiched between the can and the lead and it delivers a shock uh it's an 80 jewel shock and for those of us who may not be familiar typically most devices not all but most devices intracardiac devices the maximum icd output is 32 to 35 jewels some devices 41 but these devices can be 60 to 80 jewels and you have the issue therefore of pain defibrillators when they shock can give you a major major uh complication a major major issue with regards to post-traumatic stress disorder severe anxiety morbidity um in these patients that is is really sometimes often remarkable i had a patient who was saying that he was in vietnam and this was like vietnam was nothing compared to getting these incessant shocks and so so is there a way to shock the heart without shocking the heart to defibrillate the heart without shocking the heart and so let's take a step back and remember what why do we have to defibrillate fibrillation how does fibrillation defibrillation work the way that defibrillation works is it creates uniform simultaneous transient absolute refractoriness of myocardial tissue okay so simultaneous refractoriness of myocardial tissue if at one you have with fibrillation you have little areas we can call them wave fronts we can call them re-entrant areas we can call them however the mechanism is but think of it as electrical chaos all over the place and these regions of chaos basically feed on themselves there are little circuits that are going around and around the head catching the tail and again i showed you that image earlier it's literally that same you know the the little ripples the eddy currents of myocardial activation well myocardial tissue has a property of being absolutely refractory for about a hundred milliseconds as the sodium channel slams shut and during that period of time no matter how much activity how much electrical stimulation you provided it will not be active so how defibrillation works is by delivering that shock energy it simultaneously depolarizes the entire tissue when it depolarizes the entire tissue now you have reset the refractory period too everyone now goes on the same clock so for 100 milliseconds probably even less 50 to 70 perhaps in some situations you have absolute refractoriness nothing can get activated nothing can be stimulated and all those little re-entrant currents everywhere are annihilated they extinguish and so now nothing can feed on itself because nothing exists to feed the head no longer exists to feed the tail and so the arrhythmia comes to an end the reason the pacing doesn't work is when you pace the heart you are not achieving that depolarization diffusely at all areas it's not that you need to have that myocardium a cell a given cell cares if you shock it with 40 joules or if you activate it with five volts what it cares about is it needs to be depolarized at the same time that it's neighbor two centimeters three centimeters four centimeters is away is depolarized and pacing can't do that pacing when you pace from a site that site becomes the origin and from there the electrical activation spreads so you can't have simultaneous deep depolarization across all locations that's why you need to shock shocking does that involve so but what if you had the ability to pace from say 20 30 40 spots in the myocardium what if you had a situation where every cell was just maybe half a centimeter at most away from a pacing lead that was synchronized to pace with all other 25 electrodes in the left ventricle would that make a difference well the data the animal data says yes it would absolutely it would and there's very very strong data especially in atria but even in the ventricular fibrillation so here is and you know Igor FM off has been the pioneer in this field at wash you in st louis but here's a kind of a very nice study where you have a situation where you have ventricular arrhythmia and what's happening in each one of these is you're having pacing trains delivered followed by a shock okay so as you can tell here these pacing trains are getting more and more rapid right you can see the cycle lengths are shortening so here you have pacing and you give a one jewel shock and no success here the pacing is more rapid for more sites also and once you deliver the shock you have what we call typically a type 2 conversion there's a few beats of ET and then you convert back to sinus 1.1 joule fails here 0.24 joules gives you a type 2 success now you're pacing with five monopoles so five poles at a faster rate so again more sites at a faster rate shock 0.16 joules again it's type 2 but it converts lower energy so you went from one jewel 1.1 failing 0.24 0.16 okay here seven monopoles and you're pacing at a faster rate and you deliver 0.2 joule shock still type 2 but a much cleaner maybe type 1.5 uh conversion but it's a clean it breaks at an energy of 0.2 joules so a clinical's abstract by the same author was presented last year at heart rhythm uh taking patients who had paroxysmal aphib and they were getting ready to be ablated they took the coronary sinus catheter and with coronary sinus catheter they started pacing in multiple all all those areas at the same time and then again the same thing would happen they would either convert or the shock that they would receive was low enough that at least in the in the abstract it was said that the thresholds were sub sub uh they did not have pain but again we had you know where the patients already sedated because they were having an invasive procedure already done but nonetheless this concept is has been you know worked out by fm off in great detail there's also rabbit models of ventricular fibrillation the problem with ventricular fibrillation is the ventricle is a thicker tissue and what happens is and they know this actually from from extensive mapping the reason that defibrillation fails is typically because the mid myocardium the mid myocardial cells are not exposed to enough of the current and when that happens those little rotors everything else might be extinguished and be quiet but the little rotors kind of continue in the septum and in the mid myocardium and immediately cause immediate reconstitution of the fibrillation so again if so in these rabbit models what they did they still needed to do about four jewels to shock the ventricular for ventricular defibrillation a bigger hurdle but in humans if you could have a pacing chip that would be small enough to place say in a epicardial branch vein just like we do five french venus leads right in the for lv pacing if you had something that could be as small as a one and a half to two french catheter system that introduces a lead with multiple pacing chips on it and you place that in different areas around the ventricle you now have the ability now you have the tools to finally deliver multiple pacing impulses from everywhere but what's critical they have to be small and they have to be able to be commanded to pace simultaneously with adequate outputs and so here is where the technology actually pretend has the potential to rescue the day because what you can do is you can create a situation and again this was work with idin babakani at rice and he is now at ucla you can create these chips or nodes that are powered and commanded via electromagnetic induction emi and what happens is here is kind of one of our first studies that we did and you can see the circuit there's an antenna here so you're basically this antenna is powering the chip and or the the node and communicating with it not only commanding it but powering it and here's a kind of a rendition of the size of these chips the antenna is still you know is is going to be that right now is the biggest impediment to making these small enough to not only place and say the anterior interventricular vein but in the septal perforator until we get into the septal perforator pacing induced defibrillation will not work that is where the recurrent sources that's that's kind of the holy grail and so here you see a situation you have the chest open you can see the the coils the current iterations are much less bulky than this but you see the coils here you have two chips on the atria two chips on the right ventricle two chips on the left ventricle the led is basically a marker that it's received the signal and it's putting out electrical current and what we've done is there's an onset of a hundred milliseconds so you have a atrio ventricular synchronization and ventriculo ventricular synchronization in this pacing and this is again with six electrodes wirelessly you know again it's a big big magnet but the key thing here is we did the same with the chest closed so now what the holy grail here will be and what we are hoping and what is going to be our efforts is to be able to have a system where you can take those nodes have these be small enough that you can now introduce them into those epicardial vessels and branch vessels say put 15 20 of them especially around the left ventricle and then a system which we already have that is significantly smaller than this but nonetheless obviously and then you power these in the time of fibrillation you power these simultaneous outputs that have been as high as about two volts per node right now that's what we have at this point and then with that you create the ability to defibrillate or to depolarize simultaneously the bulk of the left ventricle and we shall see whether or not that will enable us to finally achieve what we call imperceptible defibrillation and so I started seven minutes late I uh I'm on time thank you guys very much and that's it this is the team