Christopher J. McLeod, M.B., Ch.B., Ph.D., clinical director for Cardiovascular Medicine at Mayo Clinic in Florida and cardiologist specializing in adult congenital heart disease and cardiac electrophysiology, presents on arrhythmia management in heart failure in the Advanced Heart Failure Grand Rounds series.
we could probably get started if if you guys are okay with that. Um I want to thank all of you for coming in today. It's always hard to wake up early and and hear a lecture right after a three day holiday, but um this one in particular is gonna keep us entertained in awake. Um So uh I wanted to introduce you all to dr chris MacLeod Better. McLeod is one of our electro physiologists at Mayo. He did all of his cardiovascular training and heavy training up in Rochester and is double boarded. Not only any p but also an adult congenital. Um He definitely um uh is a pleasure to work with and just a very thoughtful and methodical electro physiologist. And so um we will, we're excited to hear him speak about birthday management and the patients with heart failure. Thanks for rug. So stop me at any time if if anyone has any questions or you can't hear me or there's something wrong with the connection. Um and this is I guess the first vera virtual discussion for your your heart failure transplant fellows. Um We have a few cases to uh I don't have any disclosure. A few cases to illustrate them I think take home points. But the things I would start thinking about for when I think about heart failure and arrhythmia management, there's the bradycardia elements and I we'll we'll mention those. The atrial arrhythmia is really a big one. And so we'll start off with the case in that regard CRT and some of the important sort of take home points there. What do shocks mean for the patient and what are the important things to consider in the acute management of those patients? And then synchrony is getting a little bit more ep related. But I do think it needs to be on your horizon when you look at an S. E. G. Or someone is not doing well after getting a baby. Pvcs play an important role in the efficiency of um cardiac output and so to be aware of that and then also ventricular arrhythmias. So This first case is a case from a few years back but it illustrates some nice point. So 65 year old gentleman who had seen in our clinic and you presented with a history of having um actual valve um surgery three years prior to the visit. And he was presenting with atrial flutter Earthquoms of Dystonia and an ejection fraction of 20%. I looked back at his echoes over the years and I was Seeing him three years after that operations 2014 and uh he started off with a normal ejection fraction with by a leaflet prolapse and then a flail segment and still preserved ejection fraction. Even pre bypass. The mitral valve was addressed surgically and he left the operating room with left ventricular function pretty much intact. That was the procedure, a natural valve repair done robotically and then um an annual capacity band placed. This procedure was complemented with a left sided maze procedure. So um for this part of the procedure, the paul Marie veins are clamped by one of these. Um There's a couple of tools now but you clamp the veins and you essentially create electrical isolation of the veins. And that's very similar to what we do with a catheter ablation technique. Except there isn't really any mapping and you cannot check for complete isolation. It's just a an anatomically based procedure. Long term results for these crime maze procedures are the same if not a little better in farah to catheter based procedures but I think very much acceptable to do this kind of procedure if someone has atrial arrhythmias going into and or a history of atrial arrhythmias going into um actual valve surgery. And then also the appendage was litigated, which is also part of the guidelines. So if someone has mitral valve surgery, you can recommend or you can ask your surgeon to move ahead with this because you know that there's a very high incidence that this group of patients is gonna have atrial fibrillation later on. Um my natural um Valve repair at the time of his discharge ejection fraction 56%. And then um when I was seeing as EF had really gone down. So that's the CCG for those of you who um can't see the screen well on your iphones, I'm just going to point out the small p waves here that are marching through. These are what we would say. Um This is what we would say. Just an atypical flutter. You don't see that negative sawtooth pattern in the inferior leads. Which is not uncommon after this kind of procedure because that's a cabo trikus but is miss flutter on the right side which these cryo procedures or forest topic procedures. You can't reach to the right side. So it's very common that we do see those right sided flutters. But this is an atypical flutter. It it is not your ah sawtooth um Typical cable track has been dismissed flutter. So he has um a controlled ventricular response. It's 2 to 1 with some pvcs. Yeah those p waves that you can see. The T. Wave there is um not smooth. It's punctuated by these sharpie waves. And you can just see with very little change in his activity. We have another E. G. Hear of him conducting much quicker. So at rest with 2-1. And as soon as he was doing anything his heart rate would rapidly increase um With this slow flooded cycle length and he would go very quick. His heart red would jump up quickly. His medications Coreg 25 twice a day like this in april five furosemide and then Xarelto. So what to do here you have a patient is a few years out from a mitral valve surgery with a uh an atypical flatter. And his ejection fraction is in the 20% range amiodarone. Socal fleck. And I'd ablation or just use a rate control approach which would be rational. So um I'm gonna use this as a platform for um why we would and why we wouldn't use a Class three drug we had a we had. So it'll all there as well as amiodarone. And I think just to make sure everyone understands that the reason we would use a Class three drug or a Class one drug really just depends on the mechanism of that arrhythmia and these arrhythmias. And for all the heart failure arrhythmias, all I say, Must be 95 to even higher percentage range. Most of your arrhythmias are going to be scar related arrhythmias. That means that if you've got a ventricular tachycardia, there's scar in the ventricle either from a dilated cardiomyopathy or their scar in the ventricle from a prior infarct or these patients have had cardiac surgery before. So you've got an a tree artemis site in the atrium. So you've got the scar related flutters. And here we know this patient has had the atrium intervened upon. Uh not only to insert that mitral valve, but then also to like get the appendage and then also to clamp those veins. And so we've got scar and how re entry really works for the um mechanism of arrhythmia is just um uh detailed here on this diagram attic um slide. So if you think of a scar is sort of a central focus um where no electricity can conduct through. And then with any electrical conduction whether it be through the atrium or through the ventricle electrical activity cannot pass through that scar and it'll go around that scarred by the time it's got to the other side of the scar. If that tissue has gone through its re polarization phase it will then be able to be excited again. So if you think of the Q. R. S. And the T. Wave, if that T wave is completed you can then conduct again through that. So it's now excitable again, it's now deep polarized, its re polarized and you can then conduct again. And that's the principle here and so any tissue that has a scar can rarely be a focus for reentry. This could be an ischemic scar. This could be a valve with a scar nearby atrium or ventricular. But that's the mechanism for almost all of the arrhythmias you're going to see in heart failure patients. And then um fleck and I'd versus so it'll class one versus a class three drug um by and large for all of your patients. You want to choose a class three drug because you're going to then be lengthening out that re polarization. And so here you can see what's happening is we're changing the excitable gap that re polarization segment. If you think of the T. Wave as it lengthens with tickets and as it lengthens with so it'll all you're going to see that if there is a wavefront going around that scar it's not going to be able to re excite that area because that area um is still going through its re polarization face. So you've really shrunken that excitable gap and the longer you prolong re polarization you make it less likely for this arrhythmia to perpetuate and it just extinguishes itself. So it's a very safe way if there is not excessive QT prolongation. It's a very safe way to treat any kind of scar related arrhythmia. It really gets to the heart of the mechanism of the sky related Vts. And those are the drugs that you really want to use as a first line go to for essentially any heart failure patient where you expect there to be fibrosis not in the atrium only but also in the ventricle. It's just safer. And so you are looking for excessive Q. TC Prolongation. But that's unusual that you see that in all of these drugs we would typically start in hospital except amiodarone. But so it'll all tickets and amiodarone. Those would be your go to drugs. Um The Class one drugs um flake and I'd which was one of the options in this multiple choice would be you're going to perpetuate this you're going to slow the conduction of this arrhythmia. So it's really just going to lock into that arrhythmia. It's going to stay in that arrhythmia And you really extend that excitable gap because you're slowing production. You don't do anything about re polarization. And so what you see for the atrial flood is is that Instead of the conduction to the ventricle being 2-1. Because it's flood is now a little slow. It becomes 1-1 which is much more dangerous for the patient. And if you see any kind of, if there is any kind of scar on the ventricles and you slow that down you will start these ventricular arrhythmias just by using a class one drug. And so just making sure that you guys understand the mechanism and why you would steer away from the class one drugs. Prepa phenomenon and fleck and I'd acceleration is a little different and I would think of that as really an injunctive medication. It's not very strong injunctive to your class three drugs um and lidocaine procaine and might have got some different kind of effects. But if you really want to slow conduction it would be with the class one C. Drugs and those are the ones you would steer away from. So any structural heart disease, this is these are recommend recommendations that weren't changed in the recent update for the A. Fib guidelines. Um So first line treatment for C. A. D. It would be to Kissinger Aneta and social. I didn't mention Grenell around there just because it has um concerns and it's also a very weak agent. But I'll speak about that in a second. Catheter ablation is for patients who are failing these drugs or they're not effective or they're not tolerating them. amiodarone defer to lead for heart failure is very reasonable. But it's rare that I tell patients amiodarone is the first line drug. I really want to make sure that we're using it to stabilize that patient using it as a short for a short time period rather than committing a 49 year old with A dilated cardiomyopathy for two amiodarone lifelong, you really want to use it to treat the rhythm and then start looking at other options too. To address the arrhythmia. amiodarone is a very good agent, but especially for your boards questions don't put that in as a first line agent unless it's going to be short term therapy with amiodarone, trinita rona in both of uh the trials, looking at persistent atrial fibrillation and patients with congestive heart failure showed increased mortality. So yes, you can use it for patients with structural heart disease, specifically, rarely for those with ischemic heart disease who don't have persistent af so paroxysmal atrial fibrillation, uh and those who have paroxysmal af and heart failure, which is quite unusual, uh sorry, without heart failure. So, in structural heart disease, it really is a very small nation that is esque emmick heart disease, but increased death in both those trials. If there's a heart failure, persistent atrial fibrillation. So, going back to that patient, uh, if someone has had an ablation before or amazed before very often this is related to incomplete ablation in one area, or healing of ablation in one area. And we found when we took this patient to the E. P. Lab that there was conduction in all the veins and that there was a few gaps in these maize lines. So ablation, very little ablation was necessary just to terminate that flutter and then um patients ejection fraction climb back up into the normal range and then we stopped all of those medications. Um So just summarizing this case here, if you see someone with these atypical atrial flutters or any atrial arrhythmia and the ejection fraction has really gone down until you have really stabilize the rhythm. We would I would certainly start thinking of this as being a tachycardia mediated cardiomyopathy. That should be your knee jerk reaction because it's reversible. It's remedial to treatment and you can see that patients do well these, I'm not sure why not. Everyone develops a tachycardia mediated cardiomyopathy. You see some patients who have been taking Codec for a long time in the ejection fraction is okay, but some patients it really hurts their. Yes. And um if you're able to treat it, it's one of those reversible um interventions for for heart failure and you can get patients off some of these medicines, if not all of them. So, um, we mentioned uh in the procedure earlier on, um, that the patient underwent one of these cry amazes um this is a diagram of a complete um cox maze. One of the variations, there lots of variations in every surgeon when you speak to them, does them a little differently, but just to make you guys aware if someone has gone to the operating room and they've had one of these procedures, that one was a very straightforward one where they put clamps around these pulmonary veins. Were looking at the back of the heart and they also like getting the appendage. But otherwise they can be a lot of other lines between the bricks. Um So between ibc and spc on the right and other lines around the tree coast, but valve and going to the appendage, you can really transect the atria and also affect into atrial electrical conduction by some of these procedures. If they if they have been done in a rigorous manner or they have adhered to those cox maze principles. So if you can imagine, I don't know if you can see my cursor but I'm putting it up here near the right atrial appendage. If someone had a an atrial lead place there um And the atrial leaders pacing, it's very difficult for electrical conduction to get even to the left atrium which is the important atrium you want when you're looking at cardiac efficiency you're looking at left atrial to left ventricular synchrony. When you're considering a v synchrony, right atrial to right ventricular synchrony is not really that important but very long are A. To L. A. Conduction times. If you've had a lot of these um linear lesions done either with ablation or with these um with these lines. And so if a patient has done poorly after they're maze procedure or and the ef looks okay or done poorly after their ablation. We have to worry that we've transected or really cut up the the atria too much so that electrical conduction is not making it through the heart. You can see this. Just looking at the scg here you can see an scg of atrial pacing. So atrial pacing and this 460 millisecond delay before it gets down and causes a Q. R. S. Or results in a cure. S. Very long inter atrial conduction times. Here's another patient where april pacing spike long time to even form the P. Wave. So beyond the just be cognizant of that um Here is an electrical read out of that where we've got catheters in the heart. This is a catheter in the left atrium and we have a catheter in the right atrium. And if you look at these signals in the left atrium just on that currently sinus catheter the left atrium let me go back to the left atrium which is this signal here is being activated at the same time as the left ventricle. So if you're activating your left atrium at the same time as your left ventricle you're really not allowing time for that left atrium to squeeze and fill the left ventricle so that atrial ventricular synchrony as being curtailed or cut short by that very long delay in the heart and something to be aware of. These patients are not doing well after pacemaker implantation. You can see this nicely on the uh A. And V. Waves when you're looking at the inflow. Um And the P. Wave can be curtailed um by these long filling times. And so even if you're not looking at this carefully you should hear back from your colleagues. And these are one of the things we look look at. If someone does worse after CRT we should go back and just look at their filling. I just really making sure you guys are aware of sort of the mechanics and the mechanisms behind patients doing poorly after C. R. T. Especially if there's been surgery or ablation involved. You can just delay conduction and that abbreviate. It's filling another example of that. So um atrial fibrillation and uh heart failure. Um The more a fib you have the more you're ejection fraction can decline. And if that's the case and you're getting a dilated LV. You're going to get more fibrosis. More fibrosis is ultimately going to lead to more heart failure neuro human neural activation. More heart failure is going to lead to more atrial fibrillation. So you do want to interrupt this um vicious cycle in some way and then um makes sense to just keep these patients in sinus rhythm. But looking at the data this is the trial that was done after the affirm trial for patients without heart failure. So these are heart failure patients. When we looked at rate control versus rhythm control um keeping patients in in sinus rhythm versus just slowing down their rates with a v nodal blockers, patients live just as long. So even though it makes sense from that schematic that you saw earlier to avoid and break this vicious cycle of of atrial fibrillation, it didn't really pan out in the uh in this large multi center randomized trial. And so rate control is a very important element. If you see someone with atrial arrhythmias, the first response should be I need to slow down these heart rates to maintain human dynamics to maintain filling. If you are unable to do that, it makes sense to move on to rhythm control which would be maintaining sinus rhythm. And the reason is being why this showed that mortality was unchanged probably because of some of the um pro arrhythmic side effects of the Class three drugs. Um So tell auntie Carson. So usually starting off with a rate control if that's failing, moving to the rhythm control and making sure patients are aware that there are risks. So what about ablation then if you have a heart failure patient uh ablation uh in this new England uh trial. These were not a lot of patients were only 150 patients in this study. But you can see After ablation ejection fraction climbing up from 35% up into the 55% range. Um and other parameters of left ventricular efficiency, uh diastolic function and also left ventricular dimensions improving after a successful ablation procedure. Sorry, this was Um so 150 in total. So 58 patients in the um Sorry, only 58 patients in that entire trial. I was wrong about that. Not 150. Um So a small study and then have to be aware that in patients even you have a normal ejection fraction that if you're looking out five or 10 years that results are not that good. And so you can see um if you're using catheter ablation very often we're going to have to go back after a single procedure um and probably redo some of that or touch up some of those ablation lines, much like you saw in that initial vignette where they had been healing around some of those cry ablation. So single ablation for patients with heart failure likely is going to need some follow up later on Catherine ablation or with a class three medication. What about the role of a V nodal ablation then? And CRT in patients with heart failure. This is there have been many studies and then just exciting this meta analysis um from this Australian group which really showed significant benefit in this group. And so if someone is going to be undergoing CRT A very much prefer to move ahead with a B Note ablation. There are several studies. This meta analysis included six or seven studies. I'm just showing you one of them. This was actually out of clinic in Rochester where we looked at several 100 patients. And these are patients who did not have a navy notable ation. Those who did have an A. V. Note ablation who got CRT. And you can see a significant change in overall mortality mortality and also in those who went on to um death heart transplant to Elva. And so and this was consistent amongst all the studies that were reviewed in that meta analysis. So CRT. For patients with um Um left Bundle. Um very often um we should be going ahead with an 89 ablation in those patients you just get a more efficient delivery of CRT. And so I would be questioning CRT percentages as soon as they undergo CRT. And if you're dealing with someone with atrial fibrillation who has a left bundle who needs CRT, moving ahead with a V. Node ablation to increase the bi ventricular pacing percentage. A very recent study which I wanted to draw your attention to because it got a lot of press um last year and the year before when it really came out and there was a lot of discussion around it. Um The Castle A. F study which was catheter ablation for atrial fibrillation and heart failure patients I think for a lot of heart failure patients the study is not um suitable and I'll show you why. Um so they took 400 patients with heart failure in atrial fibrillation and they were assigned to either Catheter ablation or medical therapy and then the outcome and their primary endpoint, they met catheter ablation significantly reduced their primary outcome of death or any cause of from any cause or hospitalization, hospitalization for worsening heart failure. So it looked like a very positive study. But when you look at the design and the mechanics of the study, you can see 3000 patients were assessed for eligibility And 2600 were excluded. It's very, very stricter enrollment criteria and these pretty much exclude the majority of your heart failure patients. So who was this very small minority that was enrolled? Um, I'll show you, um, just how picky and choosy they were for enrollment in the study. But you can see there that ablation outperform medical therapy. But these patients really the ones who did well, We're class to heart failure And if you have an ejection fraction below 25%, you didn't do well with this approach. Just because atrial fibrillation tends to recur these are sicker patients. And then also the majority of these patients were not a majority. A lot of these patients had paroxysmal atrial fibrillation, which we don't see an advanced heart failure very often and they didn't have very big left atria. So I think of these patients really as being similar to that first vignette, I showed you these attacking cardio mediated cardiomyopathy. This is new onset heart failure, paroxysmal atrial fibrillation. This is not the patient with advanced heart failure who's looking at more advanced heart failure therapies that have had persistent atrial arrhythmias. It's a very select group that enabled these patients to do better. But if you select those patients carefully, um you can get a significant benefit from catheter ablation. Okay, so newly detective detected heart failure, um I would um initially atrial fibrillation with the rapid ventricular response as I said, presumes to these patients who have a rate related or tachycardia mediated cardiomyopathy until proven otherwise. And we would address that. Either with a rate control approach or if you're not able to then an anti arrhythmic approach. What is adequate rate control? There hasn't been this study in in heart failure um and it really is different for each patient. I personally have some some rough guidelines and I want patients to be um and at rest below uh in the sort of 90 beats per minute range and at rest below. But there's really no data to to guide that. Be sure that you're speaking specifically or your patient is dealing with persistent atrial fibrillation, not paroxysmal. It doesn't make sense to be using rate control for paroxysmal because you really slow down their rates too much during the day for the heart failure patients. You want to be using peter blockers anyway. But just be aware that rate control is specifically for persistent a for you're limited by your side effects. And then the Jackson uh if there are recurrent admissions for heart failure otherwise no other reason to be using digoxin these days. Yeah. So step wise approach to managing atrial arrhythmias. We're going to start off with rate control. Then moved to a class three den ablation and moving down to a V. Note. And that's uh really from your um heart failure guidelines. Okay so moving away from atrial arrhythmias and towards um ventricular arrhythmias and and defibrillators. What about ablation? Um For patients who have defibrillators uh typically we're I'm reserving these these procedures for patients who fail medical therapy. So they have a defibrillator and they're on a clause three drug and they're failing that. And then we would take them for catheter ablation. But for this trial here the smash VT trial these were patients who had secondary prevention I. C. D. S. So this makes an important point. So if someone who you're seeing who's had an out of hospital cardiac arrest or sustained VT if they get a defibrillator we rarely should do something to prevent more VT. The reason being defibrillators don't treat ventricular tachycardia. So if you just put in a defibrillator these patients are going to get sharks and sharks as you know associated with worse outcomes. So if someone has an event that that then leads to a defibrillator ablation is a very good initial step to prevent um atrial fibrillation sorry prevent shocks. Um And you can see here even survival Um ablation versus control and control here uh in this study um was no therapy at all. So they had a defibrillator But a class three drug would be reasonable or ablation for secondary prevention. But you need to do something to prevent shocks. You can't just put in a defibrillator. Um Once a patient has a defibrillator and now we're moving on to primary and secondary prevention. Um If you see they're having events recorded on their device we don't want to wait until they're having a. V. T. Store before bringing them to the lab for a VT ablation in blue. This is early ablation for patients who have ventricular arrhythmias recorded on their vice versus late. The earlier you do the ablation the better the outcomes. So less complications patients do better through the procedure they're not as sick and the success rates are better. Overall survival is better. And this has been this is be now born out in many studies. So if you see that they are getting events or events are being recorded even if A. T. P. Is effective and they're asymptomatic bringing them to the lab sooner than later is important for survival and preventing shocks. Um So this year is showing you if they're failing drugs for their um ventricular arrhythmias were not know when to wait until they're failing multiple drugs. Even if they fail a single drug, we should move ahead with a more aggressive ablation procedure. So as I said that's really my threshold on these patients. If they're failing a drug then we should bring them to the lab for ablation. And then the other one is if they getting a device for secondary prevention we must do something to prevent them getting shocks. Either a Class three or ablation. Okay another case um to get you thinking about something slightly different, 78 year old gentleman Who's asymptomatic, has a history of bypass surgery 16 years ago. An ejection fraction 30 35%. Dilated left ventricle and has been tricky allergic to pee and non sustained VT recorded on there, telemetry severe um coronary disease. Um and had an abnormal um FFR and underwent PC. I with the drug eluting stent but still has this on their scG. So um this um E. C. G. Shows sinus rhythm with a cure rest which is abnormal. But then also these Pvcs that are coming in singles and then also run of three singles run of three. This PVC is something that really should be very much aware of. These PVCS are typically not related to ischemic heart disease or dilated cardiomyopathy. These PVCS are seen in the normal heart. They are negative in your shoulder leads Avion A VL. Their positive in your Inferior leads to three Navy F. These are flat track PVcs. So these are PVCS which are readily treatable with medications or with ablation. We see we see these throughout the spectrum of normal heart and they can obviously also be seen in patients with structural heart disease. The treatment for these is uh typically be the blockers, calcium channel blockers. Class one C for some patients who don't have structural heart disease or even ablation, that's that signature here negative in A. V. R. A. V. L. And positive in the inferior leads. It's coming from some focus between these valves. Pulmonary valve aortic valve may be behind the aortic valve. There is some muscular attachments that m biologically are a little bit more rhythm a genic. And they trigger these PVCS. And if you treat these Pvcs there's good data now this is from our Rochester group showing an improvement and ejection fraction and left ventricular uh dimensions. Also if they left untreated you can develop a cardiomyopathy from them. So this patient here we used a me, what would we choose? amiodarone or catheter ablation. Um either one would be fine um for that kind of patient who's 78 years old but you want to make sure that you address PVCS so that you improve cardiac efficiency. Okay this patient, a 54 year old male with resistant atrial fibrillation had failed Anti arrhythmic drugs, three failed abrasions when we saw him And had an injection fraction of of 20%. Yeah he was taking amiodarone motto protocol and high dose along with cultism and warfarin. So very resistant arrhythmias and um still um depressed ejection fraction, moderate LV enlargement and severe generalized left ventricular heart kinesis. So that's the CCG. So still in atrial fibrillation despite amiodarone and fairly narrow QRS. But with uh PVcs occurring about 30% of the time. Three pvcs in just this CCG. So what to do here? This patient has failed in atrial fibrillation ablation three times elsewhere maze procedure. Dad into Jackson A. V. Note, ablation and pacemaker. Even an ablation. C. R. T. Um Just walking through my thinking here. Um uh my personal approach if they fail the catheter ablation even though we didn't do them three times and they're in a fib likely we're not going to have very much more success with the catheter relation uh cutting so amazed or even an epic karniol procedure. I think it's reasonable if you're in a center that does a lot of these. But just recognizing then you may interrupt electrical conduction and atrial ventricular synchrony and atrial transport. The more you cut up the left and the right atria, the Jackson is not going to add much because the patient is already rate controlled. Um Maybe not ablation and pacemaker or C. R. T. I think if you're going to a blade, the A. V. Note and the patient has such a depressed ejection fraction reasonable to put in a left ventricular lead. So we did that A B note ablation and CRT but still some improvement in ef but not back to normal. And then looking at his sgs, he's still having these Pvcs sort of every 12345 just in 10 seconds. So 30 40% pvcs. Now make sure that you're going to address those Pvcs and then looking at his holter, 30% burden of PVCS. Uh we went ahead and a belated those PVCS and ejection fraction came up to 55%. So really just illustrating the importance of CRT percentages for some patients. Even though you had C. R. T. You want to make sure that you're delivering a full complement of PV of CRT. And so this was a study from the latitude database done by Um one of our group from Rochester here. You can see even a change in mortality in those patients who had 99.9% PVC uh by v pacing. So 99% C. R. T. Vs. Even 98% 95%. So even just separating by one or 2% points you can see a change mortality. So you really want to get those Bybee pacing percentages up. And I would look at any device interrogation For these patients immediately and just make sure you're in the 99% range. If not we need to do something about the affair but we need to do something about the ventricular activity. Um I'm not gonna say very much more about the david trial other than to make you you guys aware of. The more you paste the ventricle from the right ventricular apex, the worse it is for those patients. And so if you see a patient with it repressed suggestion fraction and they're pacing the ventricle all the time in this study It was more than 40% of right ventricular a pickle pacing. It was worse survival and worse heart failure. So just make sure that you're moving towards less RV a pickle pacing or more CRT from a practical standpoint for the last couple of minutes. Um When would I admit a heart failure patient because of their arrhythmia? So drug loading obviously for atticus in because it's an FDA requirement and so it'll all, even though it's an FDA requirement we would do the same thing. It's the same incidence of torre sides with with that particular drug amiodarone. I don't typically but I would check E. G. S. Frequently. There's just a very very low incidents of torture assad's with amiodarone. Heart failure with rapid rates. As you know these patients can uh do poorly end up with pulmonary edema. So I would definitely admit that atrial fib patient. Whereas it's not necessarily the case if you have preserved ejection fraction then anyone who's had more than one shock. One shock on its own. Um It's fine for that patient to call in and we can see them as an outpatient. But more than one shock we're entering in this risk of a. V. T. Storm and more shocks is going to be very much deleterious for left ventricular function and for survival. So we want to bring those patients in and start them on a drug and watch them carefully even if it's for atrial fibrillation. So these are inappropriate therapies want to make sure they're not getting more shocks. More sharks can really hurt the lv. If you're if you do develop an electrical storm which is three or more sharks and a significant increase in death in these trials. So you have to be aggressive with bringing those patients into the hospital. Okay I'm going to wrap up here so some take home points for a fib management. Starting off with rate control. Um That would be the first line treatment and um preferable before moving on to Class three agents and then class three agents in their own or your go to treatment for any re entrant atrial arrhythmia and atrial fibrillation. And then um um For ventricular arrhythmias really we're reserving ablation for failure of amiodarone or other class three agents. And if you're seeing these events on the device, we're moving to ablation earlier than later PVcs as you saw can really affect ventricular efficiency and performance and overall ef. And so and we sort of drawn a line in the sand as anything more than 20% but it's not as clear cut as that but high burdens of Pvcs we should think of targeting but especially if they've got a poor Ef and have CRT, we want to get the CRT percentages up as high as possible. We want to admit any patient has more than one shock for atrial ventricular arrhythmias and I'll stop there. So any questions um from you guys on the call
