Chapters Transcript Video Heart Failure with Reduced Ejection Fraction: The Preeminent Role of Medical Management Dr. Herre presents guideline directed medical therapy for heart failure patients with reduced ejection fraction. I'm John Hurry. I'm the director of the Advanced Heart Failure Program. And today we'll talk about uh the role for medical management. We hear about lots of exciting things at this meeting and many people might consider this boring, but in fact, it is important. But before we get started, uh next week's grand rounds uh will be Megan Sattler and she'll be talking about updates on the new cardiac rehab program that now includes the Pritikin diet Disclosures. Are, are there? I have no conflicts related to this talk. I will discuss 1 uh investigational drugs. So any good talk should begin with a pretest and the pretest is uh what does the second m in the mnemonic most damp for the management of acute pulmonary edema represent? Now this goes back about 50 years. Uh So this is the management of pulmonary edema in 1973 which also happens to be the year that I started medical school. So take a second to look at that, come up with an answer. And here is the answer. Uh The answer is M and that stands for mercurial and that was mercurial diuretic, which was what we had for uh, the uh management at that time. Uh All of the others followed that, uh, the first M is morphine, the second M is oxygen. The third M or the, so the third S is, uh, sit them up, the T is rotating tourniquets. If you want to keep the blood from getting back to the lungs, you simply put tourniquets around D is digitalis and that one has survived. Uh A is aminophyllin. Uh You release some of the work of breathing. Uh M as we talked about is diuretic. And when all else fails, if there's too much volume, just get rid of it with it, phlebotomy. And that's where we were in 1973. But as we, as we said, uh the uh the diuretic has survived and here are just a few key points uh with the management of uh diuretic uh should be initiated promptly uh up trade, trade quickly. Uh And you must see resolution of clinical evidence for congestion and a discharge plan to gradually reduce the diuretic. But the key here is to adequately relieve the congestion that involves getting the weight down. If you look at the date of, there are a large variety of patients who go home at exactly the same weight they came in, you take a bunch of fluid off, they get a little hypertensive, somebody gives them fluid, you add it all up at the end of the hospitalization and you have accomplished nothing So it's critical to monitor the weight and relieve the congestion. So which diuretic do you use? Uh In 2023 we'll be talking about the loop diuretics. There are three of them. View Mein Fero and Torside theoretically, Torside should be the best of these as it has a number of effects beyond diuresis. It uh blocks the effect of alva stone and uh prevent against some of the uh apoptosis and atherogenesis. So, there are at least theoretical reasons why Torside should be superior to the others. So born out of that was the transform trial. Very simple trial. Uh take patients who are hospitalized and at the time of discharge, randomize them to either Torside or fero uh at uh equivalent doses, which would be 2 to 1 uh Torside toros, nearly 3000 patients, uh 37% were female. That's pretty good. They were the typical age for heart failure at 64 they were simply followed uh for mortality. And as you can see, uh over a 2.5 year period, absolutely no difference whatsoever in mortality with uh torsemide and fero, no real reason to assume that view meta would be any better. So, uh the bottom line is you can use whatever you want. Uh Let's look a little bit at diuretic dosing. Uh you can use a lot of diuretic and if you look there at the column maximal total daily dose, uh it's really up to 600 mg of fios amide 200 mg of uh Torside. One of the key differences is the duration of action. Uh poom uh is uh gonna be the most successful of these given once daily uh metOLazone. Uh Among the thiazide really only needs to be given once daily, but there's a wide range of doses of and that should be employed as needed. So let's move on uh in the medical management to beta blockers, you can see this slide is getting a little gray there on the left side. That's because this study uh was started in 1977 and published in 1983. Very simple study. Echocardiograms really weren't a big deal then. So you took a bunch of patients who had been hospitalized for a myocardial infarction And on the way out the door, you either hand them placebo or propranolol 40 mg four times daily. Uh no need for titration, hand them a bottle on the way out the door and see how they do. And this was what uh was observed in uh the Bhat trial. And as you can see, the curves diverge early. This is a mortality only study. The curves diverge early and they continue to diverge at the end of the study after myocardial infarction, there is no reason ever to stop the diuretic. The same hold or the uh beta blocker. The same holds true with heart failure. Well, that was 1983 and all the interventionalist will say. Well, now we have stents and we do bypasses all the time. So that really, that really doesn't count anymore. Uh More recent studies here in 1996 looking at Carol in mild to moderate heart failure and over a period of about a year, as you can see uh the uh probability of event survive free survival that is usually heart failure, uh hospitalization or death. You can see a substantial benefit to carve law. Now, in the era of stents. Well, we used to say that uh if your heart failure is really severe, that you're not gonna tolerate a beta blocker and you really can't do that. Uh that also turns out not to be true. Uh this was the Copernicus published in 2001. All you had to do to get in this trial was be off inotropic therapy for four days Wise, optimal medical management for 2001. And again, you can see that Carol is far superior to placebo. So uh for heart failure, it's beta blocker forever. It's beta blocker in everybody. And uh it's maximal dose. Let's look at the dose. Uh This is a, a trial uh called the MOA and it looked at a dose response for uh in this case, Carol. And uh this is over a period of about a year or, or two after uh initiation. And the first thing you see over on the left is that uh the placebo patients got better. Uh or at least the placebo patients with non ischemic cardiomyopathy got better. So we expect some improvement uh in uh the ejection fraction in non ischemic cardiomyopathy. Uh over time as you get to greater and greater doses, uh the benefit in non ischemic goes up. Whereas the benefit in ischemic cardiomyopathy seems to top out at about uh six and a quarter or 12.5 mg. But what's critical here is that for patients with non ischemic cardiomyopathy, the rise in injection fraction is uh fairly linearly related to the dose. All right, moving on to uh the next uh class of drugs that uh was introduced for heart failure. And that is the uh ace inhibitors. This was the solved study studies of left ventricular dysfunction uh again, performed in the late 19 eighties and reported in 1991 a a very solid study, 2500 patients uh about 60 years old, all had uh terrible ejection fractions. The baseline medical therapy at the time of this trial, uh consisted mainly of digitalis and diuretic uh with some vasodilator usually at nitrate. So, a good trial based on optimal medical management available at that time. And here again, the result is clear, overall mortality is reduced substantially in the patients on a Nalopril. So, this was one of the first studies that established a critical role uh for the ace inhibitors in the management of heart failure. Well, if an ace inhibitor is good, then an ace inhibitor plus an angiotensin receptor must be better. This was the val heft study Valsartan in heart failure. Now, uh and that's something you'll see as this talk progresses, the number of patients continues to get greater and greater. Uh here. Now, 5000 patients randomized uh between placebo and Valsartan. The critical thing to see here is that over 90% of patients in both groups were on an ace inhibitor, beta blockers were beginning to catch on there. About 35%. Still, two thirds of the patients were managed with dioxin and the majority with diuretic. And what you see here is that the mortality with the addition of Valsartan to an ace inhibitor uh was really uh not unchanged. Uh There is a small change in uh the combined endpoint point of death, cardiac arrest and heart failure, hospitalization favoring Valsartan. Uh But all in all in this study, the results for the addition of an angiotensin receptor blocker to an ace inhibitor are really not impressive. Uh The patients who uh clearly did not benefit in this study. Uh If you look there to their, to the right of unity, patients who were already on both an ace inhibitor and a beta blocker uh did not benefit either in terms of the combined endpoint or mortality when you add an angiotensin receptor blocker. So what about the angiotensin receptor blockers as an alternative to uh ace inhibitor. And this was the charm alternative. Uh the uh angiotensin receptor blocker in this study was canda artin again, 2000 patients all about the same age as the other studies with an ejection fraction. Here of about 30%. And here there is a fairly profound difference between uh placebo and can sarin with a substantial reduction in cardiovascular death and hospital admission. So, if you cannot use an ace inhibitor, at least in 2003, it was clear that uh an angiotensin receptor blocker was a viable alternative. All right. Well, everything changed dramatically. Uh in 2014. Uh with the release of the first of now, many trials looking at Cuba trill slash valsartan or uh entresto in the management. Uh So the previous trials established the benefit of angiotensin receptor blockers uh with a, a variety of benefits. But uh some of you have been around long enough to remember when we use Nasrat in the management of heart failure. Uh and it was miraculous except if you looked out at 30 days or so, it didn't look quite so miraculous and it went away uh about 20 years ago. But that does not mean that the natural peptides are not good, particularly when they are naturally occurring natural peptides. Uh there are a number of them uh and they are broken down by a compound that you make called Neroli. And if NAIC peptides are good, then perhaps we should block the breakdown of the natural peptides. And that is done with uh with the drug secure. It's a selective blocker of neroli and that increases the concentration of natural peptide which leads to an assortment of uh beneficial things. Vaso dili location, uh reduced sympathetic tone, reduced aldosterone levels. Uh and it's a diuretic as well. So this study uh really changed uh overnight what we do. Uh Again, a very well done study. The paradigm H F over 8000 patients with our usual ejection fraction of about 30 percent, still 80% were on diuretic. But now we're seeing uh over 90% on a beta blocker still some on digitalis, uh many on Spironalactone. And we're beginning to see the results of the trials looking at primary prevention, I CD and resynchronization. So very solid patient group and uh the results were quite clear, a hazard ratio of 0.8 for the patients. Uh On uh entresto substantial reduction in mortality. The curves continue to diverge uh at the end of the study suggesting that there is no time uh to stop this. So this was really the first big development in nearly 20 years in the management of heart failure published in 2014. Uh in the mid-1990s, we knew about pretty much the rest of them. So this, this has made an enormous difference. All right. Well, let's look at aldosterone. Alvis stone is bad for your health. Uh These are two slidess taken from a bunch of rats who uh had heart failure. One group of the rats, you fed aldosterone and salt and the other group you fed a combination of aldosterone salt and the aldosterone antagonist a plan. And as you can see in heart failure, uh the Minera coid receptor antagonists, uh at least in this country uh available on the market are plein and Spironalactone dramatically decrease the development of fibrosis that was directly related to the aldosterone. So this uh led to a study called the s very appropriately named uh 1600 patient, usual age, usual ejection fraction, everybody was on a diuretic and most patients were on an ace inhibitor. Still in the 19 nineties, about three quarters of the patients were managed with uh with digitalis again, a dramatic difference this time, all cause mortality. Uh And as you can see a substantial reduction in all cause mortality uh over a three year period with Spironalactone, I think this is one that is, is overlooked very frequently. I see a lot of patients referred, who are who are not on this. Uh It is not particularly hard on the kidneys. You do have to watch the uh potassium, but in general, uh it's well tolerated. These patients were all on more than or they were all on 25 mg a day or more. Uh I see a lot of 12.5 mg a day. There were really no data to support the efficacy of that. So, uh this, this is where we were established uh in about 2015 with uh beta blocker angiotensin receptor blocker ace inhibitor uh and mineralocorticoid antagonist. So, the next big news uh came out in uh about 2019 with the S G L T two inhibitors. And obviously, I cannot talk about all of the mechanisms for uh S G L T two inhibitor benefits in heart disease. Uh Probably the main 21 is it is a diuretic. Uh And one of the key points to remember is that when you initiate an S G L T two inhibitor in heart failure, you can often decrease the diuretic by about 50%. Uh The other, I think that is, it is at least interesting is that it has a direct effect on the myocardial sodium hydrogen exchanger. And that looks something like this. Uh The top is uh what you see in a patient with heart failure uh where A T P coming from the mitochondria uh is decreased by blocking the uh sodium uh hydrogen exchanger. Uh the concentration of A T P uh goes up. That is uh but one of many, many effects of the S G L T two inhibitors. So the S G L T two inhibitors had kind of an interesting road to being used in heart failure. Uh As you may recall uh about 10 years or so ago, it was recognized that many of the diabetic agents were actually bad for the heart with increased mortality, increased hospitalization, increased complications. So the FDA said that if you want to market a new diabetes drug that you must test it in patients with heart disease. Uh So, uh all the S G L T two inhibitors were tested in heart disease and everybody acts like they really knew this is what was gonna happen that these were really gonna be good drugs. Uh But I think if you look back uh this, this was a big surprise when in fact, if you take diabetics with heart disease or even at risk for heart disease, uh there's a dramatic benefit of with the addition of an S G L T two inhibitor. Now, we're up to 17,000 patients, uh the usual age, uh fairly longstanding uh diabetes, patients who you would expect to have heart disease, uh about 40% of them had coronary disease and about 10% had uh heart failure uh on a variety of drugs. Uh for both. And here again, in diabetics, with only 10% of them had heart failure. Uh As you can see, there's a dramatic reduction uh in the composite endpoint of death or hospitalization. So if you take a bunch of patients who don't have heart failure but are at risk for heart failure and cardiovascular death. The addition of an S G L T two inhibitor uh leads to dramatically improved uh survival Oh, well, what about uh worsening renal function? Uh that was a big concern with these drugs. Uh So in uh in the trial, there was uh what's called a renal composite. And that is uh was there a substantial uh decrease in the G F R? Did they develop new end stage renal disease and death from renal or cardiovascular causes? And in this slide that you can see that not only does it improve cardiovascular survival, but it actually improves uh survival from a renal standpoint and delays if does not, if it does not prevent uh end stage renal disease. So, these drugs are not just neutral for your kidneys. Uh They are good for both your kidneys and your heart. Well, what about the trials in patients with heart failure? And this is just some of them, I think I cut off the slide so it would fit but almost every S G L T two inhibitor that has been tested uh in heart failure has shown a dramatic reduction uh in in death and heart failure, hospitalization with hazard ratios running anywhere from 20.69 Uh to about .88. So dramatic improvement on top of uh drugs like Entresto, Carol and Spironalactone. Uh Another important point with the use of S G L T two inhibitors is when do you start them? When a patient is hospitalized with uh with heart failure, there's there's this push, big push to get them diarrheas and get them out of the hospital. But in fact, if you start the S G L T two inhibitor early on in the hospitalization and discharge them on the full dose, then there is a very early benefit. The benefit is actually greatest. The, the earlier that you started after the diagnosis, uh the drugs cause very little decrease in blood pressure, full dose. Dapagliflozin causes somewhere between a four and six millimeter decrease in blood pressure. And the benefit is greatest. Uh the earlier you start. So uh S G L T two inhibitors early and often. Uh So uh this is a, a summary of uh of some of the studies. And again, you see that uh heart failure, hospitalization reduced by 30%, uh cardiovascular death reduced by 25%. So, again, dramatic improvements uh in uh in our, one of our big markers which is rehospitalization And you don't have much time to prevent a rehospitalization. Rehospitalization was thir was within 30 days. So, starting it at a visit one month out, you're not gonna see any benefit started early. All right, now, we'll begin to look at some of the, some of the drugs that are not part of the core of uh heart failure management. And the first of those is the combination of hydrALAZINE and nitrate. Uh In the 1980s, uh the first of the vasodilator trials uh using uh hydrALAZINE and nitrate, took all comers and the results were were not particularly impressive. Those data were re analyzed in the early 1990s and it became apparent that African Americans benefited uniquely from the combination of hydrALAZINE and nitrate. And from that, uh the African American heart failure trial uh was, was born again, patients in their fifties, patients with terrible ejection fractions and on uh a variety of the uh standard therapy for the time this study was uh initiated in the 19 nineties, uh but still pretty good penetrance of ace inhibitor and angiotensin receptor blocker. If you add those two, it's 85% beta blocker. About 75% still 60% of patients on, on digital. So we're gonna have to talk about that sooner or later again using all cause mortality in African Americans, a 43% production in all cause mortality. Uh in African Americans with heart failure on background therapy of ace inhibitor and beta blocker. Another vastly under used uh medication. Uh in the trial, it was with a uh combination pill uh that turns out is very, very expensive, but you can simply give isosorbide di nitrate uh and hydrALAZINE at equivalent doses uh for uh about $4 a month for the prescription. So, uh this is one not to forget. All right. If you believe in the concept that you were born with just so many heartbeats, you do not want to waste them. It's the biggest argument against exercise uh in uh in lifestyle management. But in fact, you were born with just so many heartbeats, particularly if you have heart failure. And this is a family of curves looking uh At heart failure, hospitalization and death based on resting heart rate. And as you can see, the highest mortality and hospitalization is with the highest heart rates. It's a rather linear progression down. So it really looks like your heart rate in heart failure management should be 70 or less. Keep in mind that you're, you're fighting the sympathetic nervous system here, which is driving heart rate up. But we really ought to look at heart rates and try to keep them 70 or less often. You can do that with beta blocker alone. But sometimes you can't enter ivabradine. Evade is a very, very simple drug. It is a selective inhibitor of what we at least used to call phase four diastolic depolarization in the sinus node has almost no effect other than pure sinus slowing. Uh again, trial here, 5000 patients, uh most of them here on, on really good medical management. Uh Beta blocker ace inhibitor plus angiotensin receptor blocker was 93% still about 85% diuretic. Uh And uh still, now we're down to about 20% digitalis. Uh the drug does exactly what it's supposed to do. It slows heart rate. It's a consistent slowing of heart rate of somewhere between five and 10 per minute. And here, as you can see the composite endpoint of cardiovascular death or heart failure, admission uh is decreased dramatically with the addition of a of Vara. Uh so this drug is now indicated for heart failure, maximal guideline, directed medical therapy with a persistent heart rate of greater than 70. Well, we had to eventually get back to digitalis. Uh Digitalis has been around now for close to 300 years. Uh and it's gone in and out of favor over that time period. I recall very well an editorial in the Annals of internal medicine in about 1981 where they declared the death of Digitalis, it was gone. You shouldn't use it, it should be off the market. Uh Well, a group of investigators looked at this in the 19 nineties, uh randomized over 6000 patients. Our usual population age about 65 E fa little bit less than 30 on at least some uh guideline directed medical therapy. And what they found was that there was really no difference in mortality, overall mortality. There was an improvement in heart failure, mortality. But if you're gonna die, it really doesn't matter how you die. Um But to the uh to the point of the importance of heart failure, hospitalization, digitalis in a group of patients who had still had symptoms of heart failure on guideline directed medical therapy, hospitalization is decreased. So Digitalis probably still has an important role. Uh One thing to remember, it's a lot easier to use than you might think the dose is not 10.25 mg a day. Uh like we all thought it's really no more than 0.125 mg a day. You're not looking for a level of 1 to 2.5, you're looking for a level of 10.5 to 1. So uh the incidence of toxicity is much lower if you use those guidelines. Well, nobody believed that. So what if you take a group of patients who are on digitalis and you stop the digitalis? Uh does that make a difference? And in fact, in terms of hospitalization, it does if you stop the digitalis, they are more likely to end up in the hospital uh with a hazard ratio of 1.2, uh statistically significant, no big change uh in terms of all cause mortality as you might expect. So uh digitalis probably still has a role in patients with recurrent hospitalization despite optimal guideline directed medical therapy. Most of what I've talked about so far today involves blocking something, blocking the beta receptor, blocking the effect of aldosterone blocking uh the conversion of angiotensin one to angiotensin two. So we spend most of our time blocking something that we think is bad, but there are lots of good things that go on in the heart. So perhaps we should spend a bit of time uh stimulating good things. And this is really the first drug uh that or the first group of drugs, the soluble uh Olly cyclo uh stimulators. One of those is Vera and I don't know whether Wayne Old is on the phone but Wayne was a, a major investigator. Uh in uh in this trial, the Victoria using uh be to stimulate uh soluble Guolla cycles and increase the concentration of cyclic GMP that reduces neuro neuro hormonal activation, decreases myocyte damage, decreases hypertrophy, decreases fibrosis and decreases the effects of remodeling. So the, the pivotal trial here was the Victoria again, this gets boring 5000 patients in their sixties, all with EFS less than 30. And now we're really starting to see patients on what is, is now considered to be modern guideline directed uh medical therapy. Uh ace inhibitor plus uh angiotensin receptor nepro lysin inhibitor. Now, about 90% 90% beta locker and about 70% Spironalactone orleon. So, these are the results of the Victoria uh in the uh combined endpoint of cardiovascular death or heart failure hospitalization. Uh the hazard ratio of about 0.9 for vera. So this is another drug to think about in patients who remain symptomatic. Despite what is now really 2023 guideline directed uh medical therapy. All right. So now we get complicated here, but we're still in, in the mode of stimulating uh something that is good. And if you begin here with a, this is the myocyte contractile cycle, this is what happens every heartbeat uh at the cellular level, it begins with activation of the min head by hydrolysis of A T P. Uh and then crossbridge uh formation, you kick off the phosphate. Uh and that's when the heart contracts and then the whole thing uh occurs over again. A T AD P goes back to A T P and then the cycle uh continues. So if we can stimulate the activation of the M and head, then we should see, should see better contractile function. And this really should get to uh the problem at least in non ischemic cardiomyopathy. And this is the investigational drug that I will talk about. Uh doesn't have a brand name yet that I could find. Uh but it's Oma Mear and it is a cardiac myson activator acts at the level of the hydrolysis of the A T P kicks off the phosphate and leads to uh my act and binding. So that should improve contractility. This was the galactic trial, 8000 patients, the usual age, the usual injection fraction. Uh now on really good medical management, uh the A R B A beta locker and Minera Coid corticoid. Uh then we're starting to see a little bit of S G L T two inhibitor and now the use of IC DS and resynchronization. So you can see the evolution of the background therapy in the treatment of heart failure. Uh A lot of curves here and as you can see, they really aren't that impressive. The combined end point of heart failure or cardiovascular death. Uh It is statistically significant. The hazard ratio is 0.0.2. Uh the, in terms of cardiovascular death, no real benefit. This is the uh the first of a group of medicines just yesterday or the day before I got notification of a trial. Uh looking at another one of these, this is up before the FDA now. Uh I think the panel was kind of mixed on it. So we'll see whether this gets improved, uh it gets approved, but in fact, they did meet their end point, which was a statistical reduction in the combined endpoint of heart failure and cardiovascular death. This is a really interesting slide. At least I think uh this is kind of how they're expressing uh the effect of drugs based on the baseline ejection fraction. And if you look at the left panel, you see that the treatment effect, that is what is the hazard ratio in the treatment group. And you can see that the greatest benefit is in the patients with the lowest ejection fraction. And as the ejection fraction goes up, by the time you get to 30%, this drug has no benefit. And if you compare the drug oma camp to placebo, by the time you get to an ejection fraction of 30% placebo looks just as good. So if this drug or this class of drugs is approved, it's gonna be for patients with very, very low ejection fractions and many times those are the patients with non ischemic cardiomyopathy where you might actually expect that there can be some improvement. So I think, I think over the next few years, this is really gonna be uh gonna be quite exciting uh and something we need to keep an eye on. All right, what about drug dosing? If you discharge a patient on Carol, 3.125 mg twice a day, you have checked the box for following guideline, directed medical therapy for heart failure. And if you give 2.5 mg of Lysol, you get credit for that one too. Uh but that really doesn't work. In fact, uh if you look at all of these drugs, uh the important thing is to not to look at what's the minimum dose is the the important thing is to look at what is the dose that was used in the clinical trial uh where there is proven benefit because at the starting doses, there is no proven benefit. So uh for uh for Lice April, somewhere between 30 and 40 mg a day was what was used in the clinical trial. Low sarin, we think of the maximum dose of low sarin as 100 mg a day. The maximum dose is in fact, 100 50 mg a day. And in the trial, the average dose was 100 and 29 Carol average dose 37 a half, everybody stops at 25. You only need to stop at 25. If the weight is under 85 kg, most of our patients are over 85 kg. Spironalactone. Uh you don't see much in the way of 12.5 and tres most patients were at the full dose. Uh dale flows and most patients at the full dose, uh ivabradine, uh dioxin and vera all at uh at trial doses. So if you expect to see the benefit that was reported in the clinical trial, you must use big doses. Uh in terms of uh what are the benefits of heart failure therapy? One way of looking at that is number needed to treat. And uh all of the classes of drugs have a favorable number needed to treat in order to uh prevent death. Uh certainly at 30% six months. Uh interestingly, two of the drugs that we probably use the lease the combination of hydrALAZINE and nitrate uh and uh the Minera coid receptor antagonist, Spyro Laton and a player, those actually have the lowest number needed to treat. So, uh I think it's important uh to make sure in particular that your patient is on uh an M R A and M R A s beat out uh IC DS and M R A s beat out C RT. Don't worry, I'll offend the electrophysiologist again. All right. So, uh first of all, you know, we need to do no harm. I've talked about all the great things we need to do first do no harm is sometimes attributed to Hippocrates. It really wasn't. It was uh first stated by uh Thomas Sydenham in England in the 17th or 18th centuries. Uh And these are, in fact, the drugs that he was thinking about uh the nsaids uh rate slowing calcium blockers, that's uh tilts and frail. Um Again, back to the diabetes groups. The uh thysen Dione and the DPP inhibitors both have been shown uh to create risk in heart failure class. Uh One C antiarrhythmics, uh things like Flein, uh uh Flein. Uh This story goes back to the 19 eighties as well. Uh If nothing else, Flein gets rid of every PV C that you have. And in the early 19 eighties, variety of studies showed that after myocardial infarction, if you had a couple of PV CS or nonsustained V T, your mortality was increased dramatically. So, obviously, it made perfect sense. If mortality is increased by ventricular Opie, then mortality is reduced by getting rid of it. And that didn't work out so well. Uh mortality was dramatically increased uh by both Flein and can I and can is now off the market. So, uh those drugs are contraindicated in Verone as well. So, let's summarize a little bit here. Uh These are the four pillars of heart failure management. An R A S inhibitor, preferably entresto, an S G L T two inhibitor. The one that's available in the hospital is dale frozen and it's as good or better than any other one. So that's the one we use. Primarily, some of the insurers require that we use another one. Uh do not forget drugs like Spironalactone uh and try to use the full dose. Watch the potassium. Remember that the upper limit of normal for potassium is not five, it's 5.5 and it's perfectly acceptable to manage these patients with a potassium of 5-5.5. And finally, uh a beta blocker. So uh what I try to do is when I see a patient, this is my checklist. If there's, if they're not on every one of these, then you better document a reason. More drugs to think about hydrALAZINE nitrate has a class one indication in heart failure. E Aberdeen class two A indication deason and bar to B and uh camp is, as they say, not rated. So if we're gonna have a pre-test, then we need a post test. Uh The post test is according to the 2022 AC C A H A Heart Failure Society guidelines, which of the following has a class one indication is it C RT D for heart failure with reduced ejection fraction, an I V CD and a QR S duration of 100 and 50 milliseconds. Is it transcatheter end to edge repair uh for mit severe micro regurgitation with an E F of 20 to 50 A P A of less than 70 or an L V dimension and an L V dimension of less than seven, is it atrial fibrillation, ablation for heart failure with symptomatic atrial fibrillation. Is it guideline directed medical therapy or is it CardioMEMS for patients with recurrent hospitalization and heart failure? All of these, we do very, very commonly in this hospital. All but one is very, very expensive. And that in fact, is the one that has a guideline uh of a one a recommended uh for patients with uh I V CD. It's a two A, it's a reasonable thing to do. Uh For transcatheter end to edge repair. Again, a two A atrial fibrillation, a two A and CardioMEMS comes in at A two B in the guidelines. It is stated that it has uncertain benefits. So before you do anything else, guideline, directed medical therapy. So in conclusion, there are multiple mechanisms and we can attack almost every one of them with one drug or another drugs, targeting very specific individual uh mechanisms or effective things like Avara medical therapy remains the mainstay. And it's always indicated before you proceed to most procedure based therapies, early multidrug therapy improves outcomes and you must use aggressive dosing and I will stop there and be happy to answer any questions. Published March 30, 2023 Created by Related Presenters John Herre, M.D. Sentara Cardiology Specialists View full profile
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