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EP 101 2020: A Virtual Program for Incoming EP Fel ...
CRT-D: State of the Art
CRT-D: State of the Art
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to CRTD, biventricular defibrillators, state-of-the-art. So we'll pull up the video for Dr. Sunit Mittal from last year and we'll have a Q&A and we'll end the session thereafter. So if we can queue up the video, we'll see you on the other side. So thanks very much again for talking to me, allowing me to talk about CRT and I'm gonna start again with a case. So our case today is a 64-year-old male, he has mild hypertension and he presented with acute decompensated heart failure. The ECG show here the patient has sinus tachycardia, there's left bundle branch block and the QRS duration is wide at 162 milliseconds. Laboratory data are unremarkable, echo shows severe LV dysfunction, cardiac catheterization shows elevating filling pressures but no underlying coronary disease and he's begun on guideline-directed medical therapy. And again, Andrew highlighted this very nicely, is that it always starts with guideline-directed medical therapy. Even the patient he presented, some would argue, although on all the appropriate medications, many of them at very low dosages, lowest dose of Carvedilol, lowest dose of Entresto and it behooves us to never forget that everything we talk about from a device standpoint is incremental to making sure that patients are on optimal and maximally tolerated doses of guideline-directed medical therapy. Unfortunately, this patient, despite that, continued to have heart failure symptoms and a repeat echocardiogram showed no meaningful improvement in left ventricular ejection fraction and therefore, this patient was referred onwards for the possibility of CRT implant. Now, what is it that we're trying to do when we look at these patients? And for me, the pictures are worth a thousand words and I'm gonna try to highlight this point by using these tagged MRI images that were published by the Hopkins Group over 20 years ago. In both of these images, what you see are just the left ventricle. You see from base to apex, the green highlights the septum of the heart and the patient or the MRI on the left is that of someone with a narrow QRS complex and the patient on the right is somebody with left wonder branch block. So we play the loop on the left. You see that during a patient with a narrow QRS complex, you see synchronous activation of the, and I apologize, the videos are not looping. Is it possible to play it again? You see that there is basal to apical activation of the left ventricle, the septum and the lateral wall of the LV are activated at the same time and you see the torsion impact that's always seen in a healthy heart. When you contrast that to the person on the right, the patient like the one I presented with left wonder branch block, the first thing you see is that the heart has now assumed a shape of a football and while we may wanna watch football on the weekends, you don't want your heart to look like a football. You see the ventricle is dilated, it's more globular and if you play the loop on the right, you see the obvious desynchronization that occurs in patients with left wonder branch block. You have this swishing of blood from the septum to the lateral wall and which is the pathognomonic features of why these patients do poorly and from a symptom standpoint and why they develop heart failure and therefore this whole field of cardiac resynchronization therapy. Now it's a wonderful thing to talk about cardiac resynchronization therapy today in 2019 because many of you may not recognize that this marks the 25th anniversary of this publication, the first reported case of cardiac resynchronization therapy and this was a patient very similar to the kind of patient I presented, emanates from these really wonderful investigators in France in which they reported the use of four endocardially placed leads in a patient with refractory heart failure and a wide QRS. So they had of course the standard RA and RV leads but then through a transeptal approach, they put a lead in the LA and similarly through a transeptal approach, a lead through the LA across the mitral valve into the LV and showed by doing this and connecting this, all of these four leads into a system that they could actually improve the functional capacity of this patient. Now what was the reaction to this? Of course, very similar to this, the man with the new idea is a crank until the idea succeeds and this was basically chalked up to another great cockamamie idea from a group of people from France, right? And buried to the side but what really changed this field was recognizing this appreciation of the fact that by using coronary venous anatomy to our advantage, we could basically eliminate these endocardial LA and LV leads and do something from an endocardially based approach. Now it's amazing that we talk about the coronary venous system today because when I was in medical school, we talked nothing about the coronary venous system, right? There was some brief mention at some lecture about the coronary sinus and that was basically the end of it but today we recognize how important the coronary venous system is to the entire field of cardiac resynchronization. So I wanna first talk a little bit about the nomenclature and I think this is really, really important because I think this still trips up fellows and it is still remarkable to me how many reports we see from outside institutions describing where an LV lead is placed and yet there seems to be complete discordance between the report and what you see on a radiograph and I think a lot of that occurs because there is still confusion on what the nomenclature of defining anatomic territories are. So remember everything in cardiology is related to fluoroscopy and we rely very much on oblique views and when it comes to CRT, it's important to recognize these oblique views and we can start in this case from the LAO projection and the LAO projection is very, very important because it separates everything from the septum which you see down the middle versus the lateral wall which you'll see to the right and then you can further divide this area into these quadrants ranging from anterior, anterolateral, lateral, posterolateral and posterior approaches and again, the sweet spot of CRT therapy is trying to get leads in these lateral and posterolateral approaches where you will get tremendous separation between the anterior lead in the right ventricle, you see the ICD lead there versus the lead that you're trying to put into the LV. So again, LAO view to define lateral and posterolateral locations. We can then also look at the RAO view and the RAO view is very helpful in dividing the heart into thirds, the base of the heart, the mid portion of the heart and the apex of the heart and what's very important is to avoid leads that are placed in the apical locations of the heart trying to target preferentially leads in the basal and mid portions of the heart. So please understand the coronary venous anatomy. Now armed with these initial anecdotal reports, armed with the knowledge of the coronary venous anatomy, the next thing in the field was to subject this technology to randomized clinical trials. I'm not gonna bore you with a thousand randomized clinical trials but I do wanna highlight the two that got the field up and running and the first is Companion. So Companion was a unique trial that hasn't since been replicated because it actually enrolled over 1,500 patients to be randomized in a two to two to one fashion to receive CRT with a defibrillator, CRT with a pacemaker alone or just optimal medical therapy. Patients had to have a wide QRS, a low ejection fraction irrespective of etiology. They needed to be on an optimal medical regimen and they were really sick patients because they had class three or class four heart failure and these patients had a recent hospitalization for heart failure. This are the primary results of the study. The primary results of the study was looking at death or from any cause or heart failure hospitalization where patients needed intravenous drugs and the first thing I wanna point out is that if you look at the red, the patients who were treated medically, look how high the event rate was. At 12 months, so many of these patients actually had either heart failure hospitalization or died. This was reduced dramatically by the incorporation of cardiac resynchronization therapy irrespective of whether that was with or without a pacemaker. When we look at mortality, again, you see how high risk this patient population was. On medical therapy, 20% of these patients died at one year and this was significantly reduced with CRT and importantly, it seemed to be reduced a little bit more with CRT defibrillators as opposed to pacemakers and hence the reason why in the United States, most of these patients receive CRT coupled with a defibrillator. I think it is fair to acknowledge, however, that some still feel that there is a significant bang for the buck with cardiac resynchronization therapy alone and in other areas where cost is more of an issue, this is a viable alternative in patients. We also know it's a viable alternative in patients based on this second important study, which is the CARE heart failure study, which had no defibrillator arm. It looked at a very similar population to companion but this time the randomization was just to a CRT pacemaker or conventional medical therapy. When patients were followed over two and a half years, you see on the right, just mortality, on the left, again, mortality with heart failure hospitalization and you see there is a significant improvement with CRT pacemaker alone, both in terms of reducing heart failure but also improving mortality. Again, highlighting the fact that although the defibrillator is important, there is a tremendous positive impact to patients with just cardiac resynchronization therapy. When these studies were completed, we basically had the following pieces of information. You have a patient with a low ejection fraction, 35% in these studies. On top of that, you have a patient with advanced heart failure, heart failure being class three or four and on top of that, you had a patient with a wide QRS, greater than 120 milliseconds. You now had evidence to recommend moving forward with cardiac resynchronization therapy in these people. Of course, this then begged the question, the following questions. Number one, if this works in a wide QRS population, should it work in a narrow QRS population? There were two randomized clinical trials to look at this, RETHINK and ECHO-CRT but unfortunately, both showed the same thing. CRT in a randomized setting, not effective in patients with a narrow QRS. The second question the field asked is that if you limit it to a wide QRS population, is the benefit still applicable at lesser degrees of heart failure? So class two heart failure patients and this was looked at in RAFT and made it CRT and both of these studies demonstrated that yes, it does work in these lower heart failure risk patients, extending the population base out to patients with class two and above. So we have low EF, class two and then the final issue is this issue of the wide QRS. Now at the time made it CRT was being published, another thought process that came about and this was really something that the FDA honed in on which is, is it just the QRS width or is it the QRS width in combination with knowledge of what the morphology of the QRS complex is? In other words, is a left bundle patient with a wide QRS the same as a right bundle patient or an IVCD patient? And in fact, this additional analysis led to two very important observations. Number one is that patients with a left bundle branch block did dramatically better than patients with non left bundle branch block patterns, observation one and observation two, if you were going to have a wide QRS, the patients with the wider QRSs did the best but interestingly, when you factor both together, patients with a left bundle branch block and a QRS duration of 120 to 150 did better than patients with a QRS duration of greater than 150 and non left bundle branch block patterns suggesting this is very important and I'll show you this in graphical form. So made it CRT, the top two curves, you see how dramatic CRT is in comparison to ICDs alone in patients with left bundle branch block and if you look on the right, if you didn't have a left bundle branch block, it was kind of wash but what's interesting is and it's an important thing for you to recognize is that historically, we used to think, well, maybe CRT, remember, these are heart failure patients, they're sick, you're trying to do something for them, listen, why not give them CRT? At worst, it won't work but maybe you'll do better. What made it CRT taught us for the first time is no, actually, if you pick the wrong patients for CRT, you can actually make them worse. This is not something we had thought about before and in fact, you look at the group on the lower right, the patients with intraventricular conduction delays, these patients actually did better with an ICD than if you had a CRT. Again, suggesting for the first time, there may be signal for harm. So it's something very important to keep in mind. So where are the guidelines? This is pretty simple because in the United States, there's only one class one indication for CRT therapy and that's shown on the top. Your patient has to have sinus rhythm, a low EF, left bundle branch block, QRS duration of greater than 150 milliseconds and New York Heart Association class two or greater heart failure despite guideline directed medical therapy, right? So it keeps it pretty simple. Now, there are four class two way indications. These include patients, same patient as the patient I just described but a narrower degree of a QRS widening, a patient with a non-left bundle with a very wide QRS complex, a patient with AFib where you're going to try to get them to pace most of the time and in somebody with a low EF where you're anticipating a high degree of RV pacing which could desynchronize them and induce congestive heart failure. It is again important to recognize though that the best results are with the class one indication, that patient with the left bundle and a very wide QRS complex. Now, it's important to keep patient selection in mind because from the first studies of CRT, there's been this one Achilles heel of CRT therapy and that is the fact that there is a small number of patients with CRT who don't respond and you saw Andrew just present a wonderful case of the kind of patient we often see in clinical practice where you've done all of this and yet the journey can end badly because of the fact that you haven't sorted out through all the variables. Now it is important to talk about what we mean by non-response, because different people think of non-response very differently. So in the literature, non-response has been defined by a variety of soft clinical endpoints, hard clinical endpoints, some objective capacity, subjective capacity, and by remodeling. What does the echo look like? In Andrew's talk, he showed you that he classified the lack of response using echo data at six months. And I will argue, based on some data showing, that I do agree with that approach, that there's a lot to be said about using the echo evidence of remodeling as the surrogate for whether a person has responded or not. So if reverse remodeling is our goal, and it's our goal because we believe that reverse remodeling is associated with lower risk of VTVF, maybe a lower risk of ATAF, and all of those things are linked to lower risk of heart failure, which work in a loop system, then we have to think about the cocktail that goes into ensuring how patients achieve the greatest degree of reverse remodeling. And towards that end, I'm going to argue that the three ingredients to our cocktail are patient selection, lead position, and device reprogramming, or device programming, and device follow-up. And we're going to spend the rest of the time talking through these issues. Now, this is one of my favorite studies. And if you haven't had a chance to read this study, I encourage you to do it because it really highlights some really important teaching points. So this is a wonderful study where investigators looked at 302 patients. And these were all patients who had met classical indications for CRT therapy. These followed these patients for six months. They got an echocardiogram on them. And they divided the cohort into four groups of patients. In red are the patients who were super responders, 22% of the group. And in these patients at six months, the LV encystolic volume decreased by 30% following CRT therapy. In white were the negative responders, people we don't think about that this even happens, but yet 21% of the population where their LV encystolic volume continued to increase over time. Now, I don't have any way of knowing whether if the CRT wasn't implanted, it wouldn't have been even worse. But these patients did not have reverse remodeling. In purple are the responders, which was a third of the population. In these patients, the LV encystolic volume decreased 15% to 29%. And then in yellow are the non-responders where they didn't get worse, but they didn't get better, and they were still at 22%. Now, why is this important? Because when you look at outcomes, they're really dependent on the degree of response. Here are four indices, quality of life, six-minute whole walk test, EF, and LV endystolic volume. And look what happens. All the super responders do great, and all the negative responders do the worst, and there seems to be this linear relationship. Now, what are the clinical variables that help you determine who's likely to be a super responder? This is important because this goes into patient selection. So if you look at the yellow, I've highlighted the variables that come out importantly. Patients with a non-ischemic cardiomyopathy, much more likely to be a super responder. Patients with a wider degree of QRS. Patients with a left bundle. These themes are consistent. Patients with lesser degrees of MR at baseline. And patients with greater degrees of dyssynchrony at baseline. The five variables that seem to predict super response. Clinically, why is this important? Because if you look at the real hard endpoints, in this case, death, hospitalization for heart failure, or death, need for heart transplantation, or hospitalization, look what happens. Super response basically confers immortality. These patients never died. They never got hospitalized. They never got transplanted. It is what you want to achieve in your patients. Look at the negative responders. 30% dead, 17% hospitalized, and a third of them needing something done for them. So again, showing how important it is to know what the remodeling data in these patients are. So how do we prevent this journey from ending badly? Well, it starts off by ensuring that you've identified the right patients for CRT therapy. Again, data from MATED-CRT showing another way how important it is to get reverse remodeling. Look at what happens. And again, in this randomized study of ICD to CRT patients, when the CRTD is associated with reverse remodeling, look how well the patients do compared to ICDs. But look at the cohort of patients who didn't reverse remodeling. They may have been better just getting an ICD in the first place because they actually did worse over time. Again, showing how important this is. This isn't like they just may not do as well. They may actually do worse if we pick the wrong patients. Once you've identified the patient, of course, now it's time to get the lead in the right position. It is important to recognize that there still are barriers to getting the lead in the right position. You may have difficulty cannulating the coronary sinus, may have difficulty advancing the lead into the desired position. You may not have adequate sensing or pacing thresholds, and you may have an inability to avoid phrenic nerve pacing. And all of these are very important issues in when you do CRT therapy. Again, the anatomy is important. When we think about the lead, we want to avoid pacing the apex and therefore look at leads and technologies that allow you to preferentially pace the base. You want to be able to target the best site for pacing within a vein. And as Andrew pointed out, that his patient was enrolled in a multipoint pacing trial, you may want to target multiple sites within a chosen vein to do pacing. Again, always look at the x-ray. There are undesirable lead locations. You never want to see the LV lead behind the sternum in an anterior location. It's not going to do anything. You never want to see a lead very much in the apex where prior studies have shown signal for harm. So important to look at the lateral radiographs to have a good idea of where your lead is. The phrenic can be a problem. In 43% of cases, the left phrenic is just within 3 millimeters of the desired lateral vein. So it stands to reason that this clinically can be an issue when you're trying to promote a CRT pacing. A lot of these technical challenges have been overcome by the availability of quadrupolar LV leads. These leads have a low risk of dislodgement. Because there are multiple pacing options available, there's very little need these days to have to surgically correct or revise these leads to overcome phrenic nerve pacing. They allow you to target the sites of latest mechanical delay. And of course, they allow you to do things like multipoint pacing that were discussed in the initial presentation. What does it mean to target the latest delay? Well, this is a phenomenon called QLV, shown graphically here. So you see here in a patient who's just had a CRT implant at the time of the lab, you see a lead, surface lead, atrial EGM, RV EGM, and left ventricular EGM. You can measure from the onset of the QRS to the left ventricular electrogram. You see on the patient on the right has a much greater evidence of delay, a much longer QLV measurement. And that would be a much more desirable target to pace this patient from than the site on the left. And we can obviously rapidly determine this for various pacing locations by utilizing quadrupolar leads. Once the lead is in place, then the next stop is programming. So Andrew mentioned in his talk about what the role of AV optimization could be. Well, the AV optimization issue, despite all of these years, still remains controversial. The SMART-AV study was a randomized clinical study that I had the privilege of being involved with, where we try to answer the following in a randomized fashion is, is there a difference when the goal is reverse remodeling between just pegging the AV delay to a fixed 120 millisecond value, if you use ECHO, or if you use a proprietary device-based algorithm to tell you what the optimal AV interval would be? And what we saw is that actually in a large population of patients, it made no difference. It made no difference whether you used a fixed interval, ECHO guided, or this proprietary algorithm. Now, interestingly, in a post hoc analysis, it appeared that a proprietary algorithm may be of value in patients with a left bundle and a wide QLV measurement. And this has led to an ongoing study that patients are being enrolled in today called the SMART-CRT study, which looks at patients with the classical indications for CRT therapy. After implant, we determine the QLV measurement. And for those patients with a QLV measurement of greater than 70 milliseconds, they're being randomized to a fixed AV delay or an algorithm-based AV delay to see whether this influences a reverse remodeling or not. So the jury is still out, though I think for most people, the importance of AV optimization is a lot lower than it used to be. And I think most people are not taking the time to do ECHO guided optimization given the cost, inconvenience, and issues with reproducibility. Another issue is should we be pacing by V or should we be pacing the LV only? So here's one algorithm that attempts to pace the LV only and fuses it to native intrinsic conduction. And the idea behind this algorithm is that by doing LV only pacing, you may be actually getting better resynchronization is then possible with by V pacing. This is possible in patients who have intact AV conduction. One study demonstrated that those individuals who are having predominantly LV pacing had a much lower likelihood of heart failure, hospitalization, or death. This concept is now being tested in a prospective randomized trial, enrolling almost 3,000 patients to see whether LV only pacing in the appropriate patient can reduce all cause mortality or interventions for heart failure decompensation. So the jury still remains out. Now, the last thing is that once you have the patient selected, the lead implanted, the device program, a fundamental prerequisite of CRT is you have to have as near 100% pacing as possible. Again, Andrew showed a beautiful example of a patient in whom this was not possible due to a high degree of PVCs. It takes only a little bit of a decline in the percentage of LV pacing to start to compromise outcomes. Here's one study published many years ago showing that the minute you actually got LV pacing beyond 92%, there was a 56% reduction in heart failure, hospitalization, or death. And in fact, there've been even further studies after this suggesting that patients with 100% do better than 99 who do better than 98, really suggesting that we really gotta get as close to 100% as possible. Why don't we do that? Or why aren't we able to do that? Here are the most common reasons. Arrhythmias like AFib or PVCs like in the case example, challenges or inappropriately programmed AV intervals, and sometimes you just lose LV pacing because the lead is dislodged, the vector is no good, the thresholds are very high, you're pacing into local score or the thresholds have risen. So all of these things have to be systematically looked at at the time of evaluation, just like Andrew did when evaluating his case. But it's also important to recognize that although we focus a lot on this number, and so obviously doesn't take a rocket scientist to know that 85% is not as good as 95%, it is equally important to note that just because the device counter says 92% or 95%, that that still may not be really effectively delivering 95% LV pacing. And to highlight that, I'm going to share with you another case. So this is an 84-year-old female, hypertension and long-standing non-ischemic cardiomyopathy who is admitted with heart failure. Her medications are listed here, and this is her maximal tolerated dosages of these medications. Here's her EKG. She's an AFib. She has left bundle branch block, very wide QRS. She undergoes electrical cardioversion. Amiodarone is initiated for sinus rhythm maintenance, and she goes implantation of a CRT defibrillator. She has an early recurrence of atrial fibrillation, but amiodarone is continued because it's doing an incredible job at rate controlling her AFib. She's admitted six weeks later with another exacerbation of heart failure. Her PACER is set to a VVI rate of 60, and she is LV pacing 94% of the time. And so it's unclear to us, you know, why despite this high degree of LV pacing, she's not responding to CRT therapy. So here's her intrinsic rhythm strip. And what you see is that despite the fact that PACER is set this way, what is happening is in this patient with AFib, there are many different morphologies of QRS complexes you see. On the left, you see a number of beats that appear fully paced. In the middle, you see beats that appear to be pseudo-fused as well as beats that are fused. So a lot of pacing is being delivered. The device thinks there's a lot of pacing being delivered, but an impact on the QRS complex is quite variable. And in fact, we were able to show that there are a number of patients that although the device counters show a high pacing percentage, there's actually intrinsic fusion and pseudo-fusion due to intrinsic AV conduction. Now, why does this matter? Well, if you take patients like the patient I described and you hook them up to a 12-lead Holter monitor so you can actually template match exactly what these different beats are, what you see is that about half the patients they're getting fully paced beats most of the time and the other half of the patients actually there's a high degree of fusion and pseudofusion beats and this matters because when you look at their clinical response it's only the patients with a high degree of true LV pacing that are responding to CRT whereas patients with fusion or pseudofusion are real non responders to CRT so very important concept. So what you really want to know is not just whether a person has a high percentage of LV pacing, you want to know how effective are these LV pace beats delivered because what you really want are the patients in the green in the upper right corner where they have a hundred percent LV pacing and a hundred percent of that pacing as effective as possible. How can you do that? Well, you can do that by taking advantage of certain algorithms that look at a concept that you've discussed for three days here looking at what the electrogram looks like when you look at it from the LV cathode the pacing pole to the RV coil electrogram and when you have effective LV capture you basically have this unipolar QS looking electrogram where the impulse is going away from the LV lead to the RV lead and that is in direct contrast to the top middle where you have RV pacing where RV goes to the LV or an intermediate pattern on the right where you have a pseudofuse pattern. And so if you look for this QS morphology, you can with a high degree of precision identify whether patients are effectively pacing the LV or not and then direct your clinical management to them. Finally, once all of this is done and the patients out of the lab and you have them programmed you still have to recognize your jobs not done. Important to recognize the importance of remote monitoring in our device patients. The HRS guidelines now have a class one level of a recommendation that all patients with a device be enrolled in a remote monitoring program. And this is important because we have shown previously that when you do that you reduce health care utilization costs which is especially important as the devices become more complex. CRTD patients on remote monitoring in the US associated with a 45% reduction in health care utilization and of course survival. This is a large observational study we did where we try to determine whether or not patients with a high degree of remote monitoring did better from a survival standpoint than patients with lesser degrees of remote monitoring shown in blue versus no remote monitoring shown in red. And you see that there's a dramatic improvement in survival in those patients who are engaged with remote monitoring at a high frequency of time. So I hope I've convinced you that when it comes to CRT, it's important to identify the right patient, get the lead in the right location and think very much about programming and follow-up of these patients. The goal really should be to ensure reverse remodeling as that appears to be associated with the best outcomes and always recognize that these things are important to keep in mind because it is possible to do harm with this therapy if we don't keep these issues in the back of our mind. Thank you very much for your time and attention. I'm happy to answer any questions you may have. Terrific. We're going to answer a few questions, take a break, then we're going to come back and have another talk and then we'll see what time allows for the workshops. A couple of questions that came up that were sort of thematically related. One is a CRT-D versus CRT-P. Could you just give us an overview of when you would go to a CRT-P? Yeah, so there are a few areas in our practice that we use CRT-P. One is in patients who have pacing-induced cardiomyopathy. You have a patient that you know before they got a pacemaker, they had perfectly normal LV function. You put a pacemaker in them, they start to basically undergo obligate RV pacing. You start to see a temporal decline in their EF. There, that's a population I would do a CRT-P because it appears that you should be able to reverse that etiology in that population. Secondly, of course, it's important, this is a classic example of shared decision-making. For many patients as they're older, what they're really interested in is not just, they're mostly interested in quality of life. Remember, these are patients with advanced heart failure. They're presenting to the heart failure, many of them in hospitalized. They want that day-to-day activity, the quality of life to improve. They're not as interested necessarily in sudden death prevention as the primary thing in their focus. Even with that, though, never forget, based on cure heart failure, that there is a mortality benefit to CRT pacing. I discuss that concept very seriously with my patients. Many of them, they just want the CRT-P and they don't want the added defibrillator. This is an important and emerging area, the shared decision-making which we've talked on. There are many elderly patients in whom the quality of life is important, but living longer and compressing morbidity are factors as well. Just this month in Heart Rhythm, we published the CRT-P versus D looking retrospectively at a large patient population. Quality of life is high, survival and some of the CRT-P, which we don't have as an endpoint, but cost goes way down. It's an emerging area and it's one that needs to be considered carefully in making this decision and one that we actually got a pilot NIH study going on. Sameer Saba, one of my former fellows, has now got a pilot study going on in this in the elderly patient population. Great, and we're back. We're going to do a Q&A. I just want to point out that Dr. Mittal was very apologetic and sad that he was not able to join us. Same with Dr. Michaud. Their lack of presence today has to do with scheduling issues and our juggling things around for this virtual version of EP101. It in no way reflects their lack of interest in participating. They both are very motivated and they send their regards and are sorry they couldn't participate this year with the last minute change in format. Thanks for putting in your evaluations and we're going to get to some questions about CRT-D devices. We're going to be surrogates for Dr. Mittal in fielding your questions. One question that came up has to do with planning for CRT implantation and whether or not a CT venogram of the coronary sinus and veins is something useful and routinely done in your practice before CRT implantation. Thanks, Tasha. That's a good question and the short answer is that it's not used routinely. It's used very selectively. Early on there was a fair amount of data that came out about the use of the venogram phase of the CT scan to look at the venous anatomy. One can also use coronary angiography, particularly if there's a long shot of looking at the venous phase of it as well. But currently in almost all patients we rely on the venogram that's done of the coronary sinus at the time of the procedure itself. So it's not routine to get venograms in most of these patients, but I personally believe that shooting the venogram of the coronary sinus with a balloon catheter is extremely helpful. Shortens radiation times and really gives you a sense of the options for LV lead placement, which as Dr. Mittal indicated, are really, really key to get it basal, get it posterior or lateral. Let me actually add to that question, by the way, which came from Dr. Atif Rauf. The question is if you have a patient who already has a device and you're looking to upgrade to a CRT version, is there any role from doing a balloon venogram from a femoral access site before you go up and open the pocket to make sure that there's a target that's acceptable? It's a novel idea. It has been done selectively by some people, but we take a little bit different approach. And a couple of things we need to keep in mind is that when you have an existing system and you are going to be doing an upgrade, the complication rates go up dramatically. The REPLACE trial showed us that if you look at new implants of CRT versus upgrades, there's almost a fourfold increase in the risk of complications. So making that decision right up front, of course, is preferred, but not always possible. When we do upgrades of pre-existing systems, we take an approach in which we typically try to avoid opening pockets. So in a left-sided or right-sided system, what we'll do is to actually many times do a venogram of that arm, make sure that the vessel is patent, do a subclavian stick percutaneously. We'll frequently make a small incision on both sides of that before going in with our short introducer. And then actually getting the coronary sinus cannulated, doing the venogram, placing the lead, and then subsequently opening the pocket, making a small incision at the point where we've put the lead in, putting the suture sleeve there, and then tunneling it down to the pocket. In those instances where you're not able to get into the coronary sinus, or you cannot get a suitable vein, or you get phrenic nerve stimulation, then you've not violated the pocket, and I think thereby decreased the probability of an infection. So that's the approach to it. It's one of many approaches I know that many people... Dr. Estes, Mike just went quiet. Sorry, I can take over. Sorry, Dr. Estes, I'm not able to hear you. You can try again if we can troubleshoot that, but I can take over the discussion for the moment while that's being troubleshot, if that's in fact the past tense. One question that came up has to do with heart failure status in patient selection. Sometimes people are class three versus class four at different times, so how would you use heart failure status to pick? And I think that question has become a little bit less important in terms of how severe the heart failure is with the newer studies that have been done and the newer guidelines in place, in that we've shown benefit for patients even with lesser degrees of heart failure in the class three and four. In particular, if we use the left bundle branch block and wider QRS patient population. It used to be the case per guidelines and for the initial studies that you needed to be class three or four, and so if you were sliding between groups, that may be a little bit more difficult to do. But the bottom line is, is that because these patients with reduced EF and almost any degree of heart failure do seem to do better, it's a little bit less critical to define exactly which group they belong to. And Mark, you can always jump in. We can check your sound if it's come back, and I'll give you back the floor. Another approach that came up is why do negative responders do worse? How do they do better? How is it possible if you are having increasing synchrony, that you could actually make a patient clinically worse? And I think the answer is, is that sometimes, despite the fact that we think we're improving LV while synchrony, we are in fact making it worse than it was. And either that's because, I don't think it has to do the way the question was phrased by Dr. Narachanya. The question there was, is it possible to make a patient clinically worse? And I think the answer is, is that sometimes, despite the fact that we think we're improving LV while synchrony, we are in fact making it worse than it was. And either that's because, I don't think it has to do the way the question was phrased by Dr. Narachanya. The question there was implied that maybe epicardial pacing from the LV epicardial lead could somehow be proarrhythmic or changing repolarization, etc., which I'll mention in one moment. But in fact, if you have a patient that has a right bundle branch block pattern, a wide-ish QRS, the LV walls may still be synchronous because it's really the RV that's late. That's the part that's the synchronous. So adding another lead and doing LV pacing may actually paradoxically desynchronize the left ventricle because it actually was fairly synchronous in the first place. That's obviously the case with a narrow QRS. That's been proven beyond a doubt that even if you see dyssynchrony on an echo, a narrow QRS patient is not dyssynchronous electrically, and you can't fix their mechanical dyssynchrony by pacing them even in a biventricular or three-site fashion. So you can desynchronize people who have a QRS that is right bundle branch block or non-left bundle branch block pattern. Regarding the other part of that implication, the question, yes, some people have proarrhythmia from BIV pacing. If you pace from the LV nearer to where the scar is or on the epicardium or maybe just the wayfront direction approaching the scar, you absolutely can have unidirectional block occur in contrast to native conduction or RV pacing. It's a very small subset, but there are no question patients who with initiation of CRT end up having increased in VT, usually not VF, but usually monomorphic VT. And there are some studies, there was one out of Pennsylvania from Dr. Hemal Nayak many years ago showing some patients where this was dramatic, where you turn on CRT, there'd be lots of non-sustained VTAC, and you turn off CRT and they would completely go away. So it certainly is possible. So if you noticed an increase in VT occurrence after CRT pacing, then it's worthwhile maybe turning off the CRT for a period, doing a test trial and see if the arrhythmias dissipate. And it may be simply the lead location and the interaction with scar. Another question that came up regards CS dissections. And what do you do if you put a balloon catheter and you shoot a CS phenogram and you have a dissection? Typically that occurs because some component of your hardware you have inserted underneath the endothelium of the coronary vein. And that usually is because a balloon is advanced not over a wire, but it ends up poking into the wall of the coronary sinus body and lifts up a flap and may even exit even into the fat pad. And thankfully there is fat in that area. So usually whether it's the catheter that did it or a sheath that did it, usually a flexible tip wire usually doesn't dissect if that's what you always keep in front. So that's a good technique. Always lead with the wire. Always unsheath the balloon catheter from your CS access sheath so you're not advancing the balloon catheter out the end of the sheath, but instead pulling the sheath back over to remove it. Dr. Estes, are you back? Can you take over? Yes, I am. So it looks like we've lost Josh, and I'll take over for him. My apologies. I think we're both, Josh and I, are running into some separate issues regarding the connections. But looking at the questions here that had come in about the technique, I think Josh was commenting on that. And because I was disconnected, I don't know exactly where it finished off. But what I'll do is to take a couple of minutes here just to describe our standard approach to starting a new CRT. We always place the RV lead first. If it's a pacing lead, if it's a defibrillator lead, we place that first. Some of us in our group place the atrial lead first. Some of them leave that till later. And we get access typically directly with a short sheath, nine French sheaths, through which we put our initial introducing sheath over a dilator into the right atrium, pulling the dilator back once it's into the mid-right atrium. The next steps really are to take what we prefer to be a hydrophilic wire, the Cheromo wire, put it into the RV apex. And under those circumstances, what we do is to advance the sheath over that wire into the right atrium. And then very commonly in the RAO position, pull the wire back into that sheath and pull the sheath back with a counterclockwise torque until it has a very characteristic motion as it comes up to the annulus, just over the annulus, and then it goes into that small sulcus just underneath the mutation ridge. Very commonly, you can then advance that hydrophilic wire right up into the coronary sinus. And if that doesn't work after a couple tries, we'll try an inner sheath very commonly with a 90-degree angle. But typically, cannulation of the coronary sinus is not the big challenge. Once into the coronary sinus, we very cautiously advance the sheath into it, pulling the hydrophilic wire out, and then implanting a balloon catheter, which we inflate. We do a venogram typically with 10 cc's. And at the very end of it, we always deflate the balloon, very commonly able to see the os of the coronary sinus, how wide it is, also able to see the middle cardiac vein, which is frequently a bailout option as well. And then we'll frequently try, without a subselector, just to introduce the wire into a posterior or lateral branching up at the base. And then over the angioplasty wire, obviously introduce the lead. We always go with the quadrilatpolar lead, which gives us many, many more options. Now, my questions are not updating here, but before we got cut off, I did see a question about what do you do with this phrenic nerve simulation. And of course, with the quadripolar leads, we have many, many more options these days in terms of pacing from the most distal, mid, or the proximal poles. And in addition, we have the option of pacing to the coil or to the can as well. So almost always, we can find an option in which we don't get phrenic nerve stimulation, trying to get the lowest threshold. And frankly, our preference is to get as close to the base as possible. And under certain circumstances, we will go to specialized sheaths that are made for particularly challenging cases that have a venous selector. It's a sub-subselector. It's a system that is made by Worley. And it would be very, very useful to use. There's a variety of specialized tools, including snares for these difficult cases as well, that can be used. But that's really for the problem cases. Again, I don't have the advantage now being able to see the questions. They're not coming up. They just refreshed here. So a question here that came in, lots of people fear CS dissections with balloon venograms. Your experience? Well, it's a very good question. And the answer is that the CS dissections do occur. They can be minimized. The way that they're minimized is to actually ensure that when you put the tip of the catheter out, put it just to the tip of the sheath itself, about a third of the way into the coronary sinus, and then pull that sheath back over the catheter itself. So you're not advancing the tip that might go into the floor or the roof or the wall of the coronary sinus. And under those circumstances, it's very, very rare to have a dissection. Sometimes when you have mild staining, you can work right around it, get your wires and get your lead implanted. But if it's a larger dissection, because the blood flow obviously is coming from the coronary vasculature into the coronary sinus, the right atrium, almost always they tack themselves down. And occasionally you have to simply call it a day, bring the patient back, and put that CS lead in. The coronary sinus dissections do not lead to tamponade. One has to be very, very careful with advancing wires out very distally into the apex where tamponade can occur. Another question came up about proarrhythmia in a CRT. It was reported very, very early. It's extremely rare, but there are selected patients in whom when you pace with the LV lead and the RV lead simultaneously, one will get episodes of polymorphic ventricular tachycardia. But those are rare, and under those circumstances, you simply have to look for an alternate pair of leads to pace with or simply turn the LV pacing off. Sunit Natal gave a response to the His bundle pacing, and it's an evolving area. It's one which currently, and I'd refer you to the most recent update that Fred Cusumodo did with the guidelines for bradycardia pacing, is really not anywhere near as established in terms of the outcomes, not only quality of life and six minute walk, but heart rate hospitalizations, mortality, and importantly, the reverse remodeling. The fact is the His bundle pacing should be really reserved, I think, for patients who are not candidates for a CRT. Now, occasionally, we've taken the His bundle as a bailout in patients in whom we can't get an adequate lead position, poor simulation thresholds, inadequate venous anatomy, or even patients in whom we have phrenic nerve stimulation that can't be avoided. In the His bundle, pacing as a bailout under those circumstances might be very, very useful. In the remaining minute, Josh, I don't know if you are back and able to join in here. We've got a minute or two. I think a couple of final closing comments. Sunit Natal made the critical points, I think, that patient selection, the lead position, and the device programming are all key. With that, probably you can get about two-thirds of patients to respond. For those patients who don't respond, the outcomes are typically nowhere near as good. It's worth selectively in those patients attempting many times with echo optimization, looking at A-to-V optimization or V-to-V optimization. But as he showed in the non-responders, many times those people do poorly. There may even be a more adverse outcome in patients who don't respond, but you can select your responses based on the presence of a left bundle branch block, sinus rhythm, and non-ischemics do much better. Frankly, women do better than men as well.
Video Summary
The video transcript discusses the use of cardiac resynchronization therapy (CRT) in patients with heart failure. CRT involves the implantation of a biventricular defibrillator device to improve the synchronization of the heart's contraction and alleviate heart failure symptoms. The video emphasizes the importance of patient selection, optimal lead positioning, and device programming in achieving a positive response to CRT. It highlights the use of imaging techniques such as CT venograms to assess the venous anatomy and guide lead placement. The video also mentions the role of remote monitoring in improving healthcare outcomes for CRT patients. It explains that patient response to CRT can vary and that not all patients will benefit from the therapy. The transcript concludes by discussing the impact of CRT on mortality and heart failure hospitalization rates, and it presents guidelines for patient selection based on factors such as QRS duration, heart failure classification, and left bundle branch block presence.
Asset Subtitle
Suneet Mittal, MD
Keywords
cardiac resynchronization therapy
heart failure
biventricular defibrillator device
patient selection
lead positioning
device programming
imaging techniques
CT venograms
remote monitoring
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