[1] Everybody here’s set, all right, none of you guys I’m sitting back there. Good morning. Can you here me in the back? Yes? It doesn’t matter. I can’t speak any louder. It’s…sorry. Okay. For the usual— [2] let’s go through the usual disclosures. I do clinical trials for all three of the major... manufacturers, St. Jude, Medtronic, Guidant. [3] I’m going to try to go through some of the case studies and this is for me the hardest thing because it’s sort of a vague assignment and sort of try to talk about something without any specific guidelines. And I’m going to try to cover I guess some implant via key issues, some afib issues and then tachy detection issues. And there’s a little bit of overlap with amy but actually in a good way. So Case number one, a 56-year-old man with ischemic cardiomyopathy, EF 27%, left bundle branch block, a wide QRS, New York Heart Association Class III congestive heart failure, referred for placement of an ICD for primary prevention of sudden cardiac death and treatment of medically refractory congestive heart failure. His medical regimen includes a beta blocker, ACE inhibitor, statin, aspirin, diuretic, aldosterone antagonist, digoxin as well. He’s maintained on amiodarone for paroxysmal atrial fibrillation and he continues to have episodes of paroxysmal atrial fibrillation with a moderator ventricular response. [4] He undergoes an uncomplicated Bi-V ICD implant with the coronary sinus lead positioned in a posterolateral branch. That’s just so you guys have an idea it’s in a good spot. Following the implant he undergoes echo-guided AV optimization. I’m trying to cover all things here now. At his one month followup he reports only transient improvement in his heart failure symptoms. Interrogation of the device reveals multiple episodes of paroxysmal AF, with an AF burden of approximately 30% and only 60% biventricular pacing. [5] Your options for improving his amount of biventricular pacing? So here this device is not just a primary prophylactic device. It is a heart failure therapy and you’re not getting the benefit of all the biventricular pacing, only 60%. So you could increase his AV nodal blocking agents. Sorry. Maxed out. AV node ablation? That would be too easy. Referring physician and the patient refuse. You gotta make the cases good, okay? Increase the amio? Aah. Nice try. Intolerant to higher doses. All right. How about customization of the ICD programming? [6] So what are our choices? Well, there’s a couple of choices that sort of maximize biventricular pacing in the presence of atrial fibrillation, and primarily from the Boston Scientific-Guidant group as their ventricular rate regulation. Jamie [SP] 03:11 hits you on you a little bit of some of the slides and Medtronic cuts two aspects. One is the Conducted AF Response and then there’s the Ventricular Sense Response. [7] So Ventricular Rate Regulation, what is it? Well, it’s a programmable feature that was designed to reduce the V-V cycle in its variability during conducted atrial arrhythmias. Now the one issue---the two issues are one, you do not get biventricular pacing if you’re not pacing, obviously; and two, the left ventricle doesn’t work as well when it’s in an irregular rate. There’s various loading. It’s been well proven that if you regularize the rate you improve LV function. So for those measures both you want to have biventricular pacing, you want to regularize the rate. So what it does is obviously regularize the paced and sensed ventricular rate. It decreases the ventricular rate paced rate after paced beats. So if it starts pacing, it sees that it’s pacing and it says, okay, I’m doing the right thing, I can start coming down on my rate. It goes faster after sensed beats. So if it sees that it’s not capturing because it’s not pacing—I should use the word carefully—if it’s not pacing it says, I have to pick up my rate, and it shortens the cycle after which it paces. And you’re only bounded by the lower rate limit, the atrial tachycardia or the ATR, lower rate limit or the maximum pacing rate, which you can program in. And the idea is that they benefit from minimizing rate variations and it promotes biventricular pacing. [8] So some of the idea is that by pacing you’re actually depolarizing the AV node-His bundle retrograde and so you’re getting sort of a what we call concealed conduction into the AV node and therefore the AV node is more refractory to subsequent atrial events. So the rate actually regularizes and slows the ventricular response. [9] So this is what it looks like. Ventricular rate regulation offers wide variations. You get big fluctuations from 60 to 100 even there. With the ventricular rate regulation on, you see you narrow down your windows, you get much, more regularization of the rate. [10] Why is it useful? Well, the worse the heart, prevalence of atrial fibrillation increases as the severity of heart failure increases. The worse the heart, the more common AF is. Incidence of AF in heart failure ranges up to 50% in some series. So irregular ventricular rates for the 20% of patients with AF and heart block, that’s easy. All right? They’re going to be paced. You’ll get biventricular pacing, you’ll have regular rates. That’s the easy one. It’s the approximately 80% with AF and at least partially conducted responses that you have to optimize their programming to regular rate. And the idea of that ventricular rate regulation, it promotes ventricular rate regularity and CRT. [11] Just again the deviation in the heart rates without ventricular rate regulation. You have a 69 beat margin from low to high. With rate regulation on it narrows down to about 37. It regularizes the rhythm. [12] Conducted AF response is a very similar idea and it comes from an old study back in ’86 where if you took AF and you look at people with atrial fibrillation with big splay heart in rates, and as you pace at faster or shorter cycle lengths, the amount of splay decreases, and this has to do again with going back, it has to do with... conduction at the AV node regularizing the ventricular rate. [13] Conducted AF response. It dynamically changes the pacing rates to increase the percent of biventricular pacing without significantly raising the average pacing rate. It goes up and goes down based upon what it sees. [14] Again if you use some of the histograms and if you use some of the data from the devices, conducted AF response paces here, there’s some sense deeps and then you get the ventricular---the rate increasing at the shorter cycle length so adapting. It’s sort of like an adaptive rate response. [15] If you look with conducted AF response you can go paroxysmal AF. You can bring people from 20 to 50% pacing with really not a significant change in the mean heart rate. With persistent AF you can practically double the amount of pacing with again no significant change in the mean heart rate. Sorry. [16] So ventricular sense response. What Jamie talked about a little bit is to guarantee biventricular pacing. Again, we want to have Bi-V pacing. These are heart failure devices. So these are electrograms. You see a V-sense here, normal beep, so if there is no pacing. With ventricular sense response these are biventricular pace beeps. What happens here is it sees a native... it senses and you see it actually has two marker channels. It’s got a small marker channel, which is a sense response, and it just has V-sense, and it has the long marker channel, which is the pacing response, because there’s nothing on there to show you that it is Bi-V, that it is sense response. If you have the programmer on it’ll show you Bi-V pacing and VS at the same time, but the strip only sends VS. [17] Skipped Slide. [18] Bah. What are they backwards. Right click. [19] Great. Okay. [20] So sense response just again pace beats, sense beats, there is pacing artifact in there. You see the lines that you get the indications, short and long. [21] Skipped Slide. [22] If there’s a run of atrial fibrillation, for instance, if there’s a run that is fast from the pacing rate, it increases the amount of pacing that you see just by this sensed response. [23] And what you see is when you program it, you’ll see that it adapts, so the VV here is 1200 milliseconds. There’s a run of atrial fibrillation that’s conducted faster than the lower rate and then the device actually shortens its cycle length to increase the amount of pacing that you get. [24] Now our patient had a Guidant device and so this is what it looked like. We brought him in. He was in atrial fibrillation and this is what he looks like with ventricular rate regulation off. You see he has relatively rapid ventricular rates. He’s got one V-paced beat with ventricular rate regulation off. We turn on VRR and we dramatically increase the amount of pacing that he gets of biventricular. So after this in the followup two months later he feels largely better with some improvement in his heart association classifications. [25] Okay. Second case. A 28-year-old male with a non-ischemic cardiomyopathy, ejection fraction of 5%, New York Heart Association is Class III, morbidly obese, left ventricular diastolic dimension 9 cm, that’s as big as my kid’s head, narrow QRS, no evidence of dyssynchrony, chronic renal failure, dialyzed through the left forearm AV fistula. It’s your worst nightmare. [26] So you smartly pass your case on to your junior colleague. But he is smarter than you, though, and he schedules that day off to close on his new mortgage because he knows that that dentist, you know, that that using that having to go to the dentist thing, that’s not going to work to get out of this one. All right? The mortgage, you know. So left with no alternative, what can you do to maximize your chance of winning, and here winning is achieving adequate DFTs and closing with the patient still alive. So the first caveat: there is no ideal configuration that’s guaranteed to work. Defibrillation’s just a statistical event. Just when you’re expecting difficulty, the more options the better. Bad heart, renal failure, big body, those are some of the factors that lead to high DFTs. [27] So what do we do? Well, you know, there’s a bunch of different programming issues about how to deal with sort of optimizing yourself with defibrillation. And so there’s using the RV Anode and DFTs. This is always whether you should make it RV positive or RV negative. And if you look at the numbers that 88%, about 90% actually do better with RV positive, but there is still 12% who do better with RV negative, and this is the whole idea about standard polarity, reverse polarity. It depends upon who the manufacturer is, about whether they---what their standard is. In general, everybody is pretty much moving now to pro---to making the default RV positive. [28] Right sided implants. We know the DFTs are a little bit higher. Left side is more ideal. You can get safety margins. In one study by Varma 10 jules safety margins were obtained in all patients, but only after optimal lead configurations. DFTs greater than 30 jules in three patients with dual coils. DFTs were less than 10 jules in 77 patients when optimal configuration. And here’s the thing. Dual coil was inferior to single coil in six patients, superior in three patients. SVC coil exerted a detrimental effect in about a third of the patients and improved DFTs in 15%. So it’s not clear that having that SVC coil necessarily improves your defibrillation. [29] So the SVC on/off programmable shocking vectors—St. Jude you can do this electrically. You don’t have to take out the pan and cathet and put a dead man into the receptacle to port, a port plug. But there is still conflicting evidence as to whether there’s any difference in DFTs between dual coil and single coil. [30] We have a bunch of studies, Gold, they found the dual coil configuration was better, 98% versus 88% compared to single coil. Again Gold low and the high proximal coils were lower than single coil so they found dual coils better. Then we have a couple studies showing no difference between duals and singles. So the idea is that for individual patients, different configurations may be successful. It depends how much you need to try and how many different configurations you want to try. [31] Tilt. Tilt, I guess, is sort of a going back to programming tilt. Back in the old, I guess, the days of PCDs. We used to sit there and measure the impedance and then calculate tilts in the OR with the surgeons, I guess 15, 13 years ago. And tilt is important because it has to do with how you’re releasing energy during biphasic shock. And everybody’s biphasic. Nobody’s really using monophasic delivery anymore. Biphasic is just much better. Pulse width example for a 65% tilt—what it does, it’ll deliver 65% of the energy and then will go to the second phase and do the same thing on the second phase, will be 65. Never goes all the way down to zero. [32] Clinical studies. No one tilt is optimal. Again it’s the same thing. There’s no one sort of one-size-fits-all. And the technology is good enough that you can take stuff out of the box and for the average patient you’d be able to make DFTs with a minimum amount of testing, but there are the outliers for which you may need to optimize, and it’s very, very individual. So here 53% had a lower DFT with a 50% tilt, 20% with a higher tilt. So again, it varies. And again, some of the devices have fixed tilt and that’s it. They’re programmed to do 65% or 50%. St. Jude actually has a programmable tilt. They have four choices of tilts that you can use. [33] Pulse width. Again, important to defibrillation. We sort of had a period where we didn’t look at it. We had a period where we looked at them back in the old days. The period where we didn’t look at it and now we’re coming back to looking at it. Programming tilt doesn’t necessarily provide optimal defibrillation pulse widths, though, and you have maximum control of the delivery of the shock because the pulse width in each phase is programmable. So it’s all about delivery of energy, and you get your maximal amount of ability to optimize and control how the energy is delivered by controlling tilt and pulse width. [34] Again so here we go, clinical studies, optimizing the defibrillation waveform results in a lower DFT. This seems more pronounced in a high DFT patient, so the worse your DFT, the more important it is to be able to optimize. [35] And there’s always those arrays, you know, those sort of things that you go into regions where you don’t like to be. It’s like along your posterior---you’re in the posterior part of the back, you’re on the side, you’re putting extra things in. They work by changing the shocking vector, but more so by changing the pulse width through impedance. So the lower the impedance at any given voltage, the higher will be the current flow. So it’s how a coil works. It can result in pain. We sort of leave it as a last result and I actually have not used a coil in years now. And you can actually duplicate its efficacy, you may be able to, by programming pulse widths. [36] So how to manage high and/or really or rising DFTs. High energy device, start with it, and then where there’s a difference between stored and delivered, some manufacturers, their devices they list as stored, so Guidant for instance has a 41 jules device but that is what is stored. Medtronic is a 35 jules which is what is delivered. The 41 and 35 are roughly equivalent of what is delivered. The Atlas from St. Jude is actually a 36 jules delivered and a 42 jules stored. Roughly they’re all the same at the high end. RV anode is optimal polarity. No one value tilt optimal. Pulse width programmability may lower DFTs. And there’s no real good evidence as to which shocking coil configuration is optimal. [37] So we underwent placement of a single chamber single high energy St. Jude ICD dual coil via right cephalic cutdown. We failed with both standard and reversed polarity. We then disconnected the SVC electrically. One adequate test and then we failed again. [38] And then we bailed for the day. Sometimes the better part of valor is knowing when to get out before you hurt someone. And so, you know, we went with St. Jude because we had a lot more options in terms of programmability primarily anticipating something like this. So we had the availability of programming pulse widths, tilt, and we knew we’d have that. So we brought him back the next day, tested with the SVC electrode out, and again with optimization, changing tilt and pulse width, were able to get a successful DFT. [39] So. Caveat two: DFT is a statistical event, not static. Changes in heart failure status, renal failure, medications including amiodarone and Coreg, all adverse---can adversely affect threshold. And as devices continue to shrink in size, programming options such as tilt, pulse width, may become much more important. [40] All right. I got 20 seconds and one more case. So I’m going to go through it [41] real quick... No, not that quick. How’s that going to sound on the tape? Okay. Fifteen-year-old girl complains of multiple episodes of dizziness. So we’ll go through this quick. First episode following recital, a month later running down a staircase, four months later at school called to the front of the classroom, subsequent episodes of syncope occurred at a basketball game and a friend’s house. [42] The pediatrician thinks it’s vasovagel. So a second evaluation includes a brain MRI, EEG are normal. Tilt table testing is normal. The patient had a little dizziness with a change in position. The patient’s mother, though, who happens to be a doctor, thought there was a brief heart rate up to about 250 at the end of the test. The physician who did the test recorded it as a motion artifact. And since that she’s had about one episode of syncope per month. It’s---each episode has been in the setting of stress or exercise. [43] She’s on Toprol XL. She did better with a beta blocker. Family history is pertinent. Her father has had three-four episodes of syncope over the last 20 years. He’s got, again, normal heart, but again, the only thing he had was a stress test with---which was normal except for frequent PVCs with exercise. [44] So this is this girl’s baseline electrocardiogram. No pre-excitation. The QT is not long, really essentially normal. [45] We put her on a treadmill and we start seeing these frequent PVCs. Some really look unifocal and then you start seeing stuff that looks more multifocal. [46] When you get her up to peak you have salvos of VT with a couple of sinus beats in there. [47] So this is catecholaminergic polymorphic ventricular tachycardia. It’s also known as familiar PMVT. They have polymorphic VT with physical or emotional stress. They have normal hearts, normal QT. Onset is really very, very reproducible during stress testing. Serum catechols are normal, so it’s like there’s something wrong with how they handle normal adrenergic sound and it has to do with calcium loading. [48] So she’s getting an ICD but there are a lot of considerations. I’ll try to go quick, I’m over time. Leads—I want something that’s coated. She’s 15 years old. She may be having extractions down the road. I want something that’s coated to prevent tissue ingrowth, make it much more likely to be extractable in the future. I want something that is small but lasts a long time. All right, I’m here, I want to protect her. She has no heart failure, no pacing indications. All I want to do is protect her from dropping dead. And I want extended detection times because she’s going to have VT. There’s no question in my mind. I just don’t want her to die, all right, and so I must be able to let the device see some VT but not necessarily treat everything. [49] So Medtronic—skip a lot of the stuff—you can do their VT detections up to 100 beats. Remember VT detection is all one beat out, start the counters again. VF, you can go up to 160 beats total, has to see 120. Not bad. [50] They have combined count counters. [51] Guidant—detection is eight or 10 beats. You can program the zones. The Zone 1 when they have like a VT zone 1. You can make it up to 60 seconds before therapy. The second zone is really only up to 30 seconds, and in the VF zone you really only have a maximum delay to therapy of 15 seconds. [52] St. Jude—VT zone is up to 100 intervals. The VF zone is eight, 12 or 16. That’s it. And so there’s a little bit less programming considerations there. [53] Just so we have an idea—if you look at these cases study following these people, you know, the mean followup—they have syncope and they have sudden death. So we know that she is at risk, but I do not want to make this 15-year-old girl crazed by getting shocked, and you guys know there’s nothing worse than somebody who’s been shocked multiple times. I mean it’s really bad when it’s very often and it doesn’t need to be done, but even with VT, invisible. They hate you and they’re miserable. I can’t deal with being hated. [54] So we went with the Medtronic Entrust VT zone, 76 beats, VF zone there. [55] She underwent stress testing, went for six minutes, frequent runs of polymorphic VT, detection criteria not met, we were all happy. A week later she was startled by a doorbell, complained of dizziness and gets a shock. She becomes more anxious and experiences multiple shocks. [56] Here we go. VT. Here’s my ATP. I got seduced by the technology. MVF. All right. So I turned her VT into VF and I made her miserable. So we reprogrammed her, turned off all ATP, turned off the VT zone, gave her a VF zone real fast, gave her a reasonable detection. I mean, you know, you gotta have some modicum of mediumness here. [57] Beta blocker was increased, maximum dose. She’s on 200 of metoprolol. Went for 16 minutes on a treadmill now. Peak level she started saying, I feel them, and she had PVCs. I stopped the stress test. Mrs. Bernstein didn’t raise a stupid boy, okay. And she’s been asymptomatic since and has had no event detections on subsequent ICD interrogation. Okay, with that I just wanted to say I want to thank Anya... one of our fellows, for helping preparing these things, and that’s it. [58]

Neil Bernstein 157ABC Case Presentations of Interest Customization for Optimal ICD Programming: Troubleshooting and Case Presentations