Medical Lectures

Practical Tips in the Diagnosis and Management of Heart Failure

Get Practical Tips for the Diagnosis and Management of Heart Failure from Mayo Clinic's Tyler J. Peterson, MD.
February 24, 2022
Tyler J. Peterson, MD

In this blog, you will learn about:

  • Giving some insight into making the diagnosis of heart failure
  • How an ECHO is important in guiding therapy
  • Patients with systolic dysfunction, or heart failure with reduced ejection fraction Deciding which medications to start first 
  • The importance of up-titration. 
  • Choosing when to add additional agents such as spironolactone and or a neprilysin inhibitor. 
  • When the systolic function improves. 
  • How long does tubing need to be continued and what can be stopped? 


So let's start with, number one, making the diagnosis of heart failure, and the importance of an ECHO and guiding therapy. What is heart failure? And I'm going to give you two definitions here. The first is my definition, and I just define it as an ability for the heart to keep up with the demands of the body. The second definition comes from the heart failure guidelines, which describe it as a complex clinical syndrome that results in many structural or functional impairments, ventricular filling, or ejection of blood. 

Now, making the diagnosis of heart failure is a challenging diagnosis. As you'll notice in the definitions that are used when they do studies on heart failure as a clinical reference, there is also what's called the Framingham criteria here. 

And you'll notice that there are many things on this slide that allow you to have both major and minor criteria. And to be honest, I don't use this slide. I tend to more think about heart failure as a syndrome of several different things that come together. 


And to go through those: so first, it's a syndrome of shortness of breath or dyspnea and fatigue. And often, there are signs of fluid overload with that. It typically improves with diuretics, and it is by and far a clinical diagnosis. The diagnosis should be made based upon the history and the physical exam. And then you can use supportive testing, such as an NT-proBNP, a chest x-ray, an ECHO to help that. 

Some of the signs of heart failure are more specific than others. One of which I like to point out is orthopnea. Orthopnea, which is getting more short of breath when you lie flat, is quite specific for heart failure. And if a patient tells me that they have orthopnea, and it sounds like they really do, then I think it's heart failure until proven otherwise. 

As we go through this definition, one of the things I want to bring home to you is that this is really a constellation of symptoms. And no one test tells you if there is heart failure.


So sometimes I'll hear people say, well, get an ECHO and see if there's heart failure. And we'll go into that a little bit further coming on. Or, you know, the NT-proBNP is elevated, then there must be heart failure. 

I would argue that there is no one test. There are multiple different things that you as the clinician bring need to bring together. And again, you're looking for that syndrome of dyspnea, of fluid backing up, of better with diuretics, and looking for supportive signs and symptoms, using your clinical skills and tools to make that diagnosis. 

And it's not always easy. One thing I want you to notice is that an ECHO is nowhere in the Framingham criteria, and has not, so far, been included in really anything I've talked about for the diagnosis of heart failure. It is very helpful in the diagnosis of heart failure because it gives you understanding into the potential ideologies as well as it has is very important in deciding how to treat that patient with heart failure. 


Next, I'm going to give you a case, we'll briefly go through and we'll use that to illustrate the importance of how the ECHO is needed. So, we have a 48-year-old male who's been hospitalized for dyspnea and lower extremity edema. He's got orthopnea; elevated jugular venous pressure; pulmonary edema on the chest x-ray. And he has a brisk improvement in response to diuresis. 

So this guy he meets, by Framingham criteria, by the definition we've talked about, this man has heart failure. And next question is, well, how do you know how to treat this patient? Do you give him an ACE inhibitor right away, a beta-blocker, spironolactone, and argue that you don't know how to treat – and you don't know how to treat until you've done another test. And that test is to do an echocardiogram. 

The one on the left is someone, who has preserved ejection fraction, and the one on the right is somebody who has reduced ejection fraction. And either one of these ECHOs could belong to this patient. And so you don't know until you do the ECHO when someone you make the clinical diagnosis of heart failure. You do an echocardiogram. 


An echocardiogram can give you insights into why someone has heart failure, such as valvular heart disease, pericardial disease, infiltrator disease. But the biggest thing I think that it often does is: it helps you to decide whether or not you have heart failure with preserved ejection fraction. So, the ejection fraction is normal or near-normal, or you have heart failure with reduced ejection fraction, where the ejection fraction is typically less than 40%. 

And you can't tell based upon the NT-proBNP, the chest x-ray, typically, the physical exam is very hard to tell which one of the categories that somebody is in, and knowing which category that's someone's in, is instrumental in deciding how to treat. 

For heart failure with preserved ejection fraction, we have done multiple randomized controlled clinical trials looking at all sorts of different drugs, including ACE inhibitors, including beta-blockers, nitrates, including spironolactone. And none of those has been shown to have a clear benefit for patients with heart failure preserved ejection fraction. So, the mainstay of therapy for someone who has heart failure with preserved ejection fraction is diuretics to keep fluid off and blood pressure control. 

We hope that, in the future, we will have more, but it is relatively simple and in some ways to treat these patients at this juncture because we don't have much that works. And I want to juxtapose this with heart failure with reduced ejection fraction. 


As seen on the slide, we have multiple different drugs that have been shown to be helpful in both mortality and morbidity. And these would include beta-blockers, ACE inhibitors, angiotensin receptor blockers, aldosterone antagonists, and neprilysin inhibitors. And we'll go through how to use some of these. 

Because we have so many more arrows in our quiver with heart failure, with reduced ejection fraction, we're going to spend the remainder of the talk focusing largely on how to treat people with this specific condition. So now we've gone through the first objective and now we're going to talk about in-patients with systolic dysfunction, or those with heart failure with reduced ejection fraction, deciding which medications to start first and the importance of trying to up titrate those. 


So, now, we're gonna go back to a case again, a 48-year-old man who has an E.F. of 28%, or an ejection fraction of 28%. He has non-ischemic cardiomyopathy. He's New York Heart Association Class 2. Here's his medications with atenolol (25), lisinopril (20) once a day, and furosemide. And he has a blood pressure of 122 over 76 with a heart rate of 68. And he's euvolemic. Here's his potassium, which is 4.4 and his creatinine is 1.2. 

And the next question be, what is the next best step regarding his medical therapy? 

A) start sacubitril/valsartan, 

B) titrated atenolol to a goal of 100 milligrams daily, 

C) transition atenolol to metoprolol succinate titrate to goal dose, 

D) titrate lisinopril to a goal dose of 40 milligrams daily; 

E) start spironolactone

F) no change in therapy. 

Not an easy question and I'm actually not going to answer this question right now. We're gonna go through a few more slides and then we'll come back to this. I think it will be more apparent. 

Alright, so when we talk about treating heart failure through reducing ejection fraction, my next goal is to run you through an algorithm of the basics of how do you move through this practically?


And if a patient comes to you, and they have heart failure with reduced ejection fraction, the first thing you want to do: is if they're volume overloaded, then you want to treat it with a loop diuretic, and you want to get that extra volume off. 

And you do this for a couple of reasons. The primary reason means that they're going to feel so much better. And so oftentimes the first time I see someone in a clinic and they have heart through reduced ejection fraction and their volume is overloaded, I will double or triple the diuretic and have them come back in a week. And by that time, they've typically lost 5-10 pounds. Typically, they're lying flat at night and they can walk into the clinic often without having to stop and they feel better. 

And now, you've got someone who's gonna trust you as you move forward with further therapy. So, loop diuretics instrumental right away. Just some practical tips on using loop diuretics. It's OK to use furosemide if that's working well. I often find that if furosemide doesn't seem to be working well, I'll switch over to torsemide. 

If that's still not working, well, then I'll up-titrate the dosage. If that's still not working well, they'll typically add on a thiazide diuretic. But I do want to caution you about the use of metolazone. 


Metolazone is a thiazide diuretic that when used in synergy with a loop diuretic is very powerful. And I myself have sent patients into the hospital after doing this with sodiums that were incredibly low or potassiums. 

The chances that you can have severe electrolyte disturbances with metolazone is significant. And so if you're going to use metolazone, I would suggest you use it in the hospital. Otherwise, if you're going to use it as an outpatient, I would use it for one, maybe one or two doses and checks like checking labs and close follow-up. 

I would really try to stay away from giving someone a week or two weeks of metolazone straight. I think that there's a high chance that you can hurt a patient that way. The other thing that will often add on if the loop diuretic is not working well is to add on spironolactone. 

It works in synergy with the loop diuretic, and it also can help with keeping the potassium up to a reasonable level because it is a potassium-sparing diuretic. Alright, so going back to the foundations of heart failure with reduced ejection fraction. So first, if their patients are volume overloaded, we treat them with a loop diuretic. 

Once they're euvolemic and stable, then we want to give them an ACE inhibitor. And if intolerant an ACE inhibitor, you would choose an angiotensin receptor blocker, and you want to start a beta-blocker also. 


So, let's talk about each of these in turn. So, an ACE inhibitor has an interesting story behind it. This is the first drug approved by the FDA that came from a snake's venom. So Brazilian pit vipers, when they bite their prey, the drug in their venom can cause hypotension and venous dilatation. This was subsequently isolated and used to create captopril. So, ACE inhibitors should be used in all patients who have heart failure with reduced ejection fraction regardless of symptoms. 

New York Heart Association Class 1 to 4. It improves most more, both mortality and morbidity, and an ACE is generally preferred. And if not, again, you can choose an angiotensin receptor blocker. Let's talk about beta-blockers for a minute. 

These are also are indicated in all New York Heart Association classes for patients who have heart failure with reduced ejection fraction. These also improve mortality and morbidity. As opposed to ACE inhibitors, where it doesn't seem to matter whether you choose one or another in beta with beta-blockers, there are three preferred agents, and these are carvedilol, metoprolol succinate, and bisoprolol. 

The reason that we choose these is they have the best outcomes and are the best studied in patients with heart failure with reduced ejection fraction. So, you should try very hard to get your patient on one of these three drugs. And as a practical tip, metoprolol succinate and bisoprolol all tend to be less vasoactive than carvedilol, meaning that if you're worried about a patient having hypotension, this tends to cause less hypotensive effect. 


And I think it's important to not only to talk about that we that these affect morbidity and mortality, but to say how much do these affect morbidity and mortality? What am I going to get my patient by starting them on these drugs? 

And if you take a patient who has baseline survival of one year with heart failure through reduced ejection fraction, and you look at that patient at baseline, on the top in blue, they have about a one year on average lifespan. 

If you add an ACE inhibitor, you can see that you get up to about a one-and-a-half-year average. And if you add a beta-blocker, you over double their life expectancy at that point. So number needed to treat to prevent one death over three years with ACE inhibitors is 26 and with beta-blockers is nine. So, these are pretty good numbers needed to treat based upon clinical drugs. 

There's also a reduction in hospitalizations. So, the relative risk reduction with hospitalization, with ACE inhibitors is 31%. The relative destruction of the beta-blocker is 41%. It's important to note, though, that these benefits were observed when patients were up-titrated to a goal or maximum tolerated dosages. And we'll talk about those. 


When we look at what is the goal dose, here's a slide, more for your reference about ACE inhibitors and angiotensin receptor blockers. And what these do is this slide does as it goes through each of the drugs in talks about what is the goal dose and what was the mean dose used in clinical trials. 

It's not enough to start the patient on two and a half milligrams of lisinopril, or five milligrams of lisinopril and then leave them be and say, yes, they're on an ACE inhibitor. These benefits were associated with the up-titration of these medications as you can see in this slide. 

Same thing for a carvedilol and metoprolol succinate and, again, showing you the goal dosages here and some slight variations. Again, another slide for your reference. And bisoprolol is really similar to metoprolol succinate. One of the things that is important, as I've just mentioned, is that "Drugs don't work in patients who don't take them", as C. Everett Koop has said. 

So, not only is it important to get them to higher dosages but also even just to get them on the drug.



Here's a look at the proportion of patients with reduced ejection fraction who are receiving gold-directed medical therapy. And about 80% of patients are on an ACE inhibitor. And about 60% of patients are on a beta-blocker who have heart failure reduced ejection fraction. 

And it's interesting to look further and then say of those patients, how many are within the goal or the target of their dose? And that goes down even more. Only about 35% of patients, who are on an ACE inhibitor, actually get to goal or target dosages. 

And only about 20% of those with beta-blockers. And so you say we've got this great therapy that can only double your life expectancy. But we're not doing that well with it. Not all of our patients are getting on it and not many patients are getting titrated up to goal dosages. And so why are we not doing better? 

And I think that this has several different issues. One is doing this hard work. But this is time-intensive; it takes resources. There's often a lack of infrastructure within the clinics to deal with this. And you can even argue about best practice alerts, which alert us to some things when I think that these things would be great best practice alerts. 

And they're not alerting to other things that may be more helpful. Other factors are things like inertia. Your patient's doing pretty well. You don't want to change anything or even the fear of harming a patient. So, you know, the patient already has a mild abnormality in renal function, do you really want to move that ACE inhibitor up? 


In general, one thing that I would like to bring forward is that when you think about the ACE inhibitor or beta-blocker, one question that comes up is: Which one do I start first? And I'd argue that this doesn't really matter. You know, there are multiple different variables, such as blood pressure, heart weight, renal function, and potassium that go into this. But what I would make a key point in saying is that don't titrate one class to a maximal dosage at the expense of not starting the other classes. 

We'll often start a little bit of an ACE inhibitor and then come back in a couple of weeks and add on a little bit of beta-blocker and we'll start to slowly climb each of those medications. We don't try to do one at the complete expense of the other. 



Here are just some general tips to optimize medical therapy in the practice. One is we generally go slow. This is not something that you're going to do in one or two visits. This typically takes, I tell patients, that we're going to increase your medicines over the next couple of months. We make small incremental adjustments every one to two weeks. 

So, for example, with metoprolol, a practical way to do this is to start 25 milligrams. And then in two weeks, increase another other 25 milligrams to 100 milligrams and then try to do 50-milligram increments every two weeks to 200 milligrams. 

Sometimes, the patients aren't tolerating it or heart rates are getting quite low. Then you might have to go slower or stop. The goal with the medicines is to give them the benefits, not to make them feel worse. And if a patient does feel like things are markedly worse on the medications, they're feeling like they're dizzy or lightheaded or unstable then it is reasonable to back down on that dose. We do not want to give people new problems. Lisinopril we'll often start five milligrams, and increase in five-milligram increments every two weeks to about 20 milligrams is a reasonable goal dose. 

Some of the tips for also for optimizing that in places where this is done well is that there's typically is a protocol that does require nursing support, which I know is not available for many of you. And many of you do not have a protocol to do this. If you do see patients with heart failure. This does ease things very much. 

The protocol that we use at Mayo, just to give you an idea, has certain parameters that the nurses will follow. And as long as blood pressure and heart rate and creatinine and potassium are within the goal, then they will increase the medications. 


Another practical tip is to tolerate asymptomatic hypotension. We routinely tolerate in our heart failure patients blood pressures of systolic of the 90s and even the 80s. The protocol that we use suggests that it's reasonable to up titrate as long as the systolic blood pressure is typically above 80 and the patient is asymptomatic. 

So, I would encourage you that if the blood pressure seems a little bit low, and it is lower than many of your other patients. But that's where we want these patients to be: 90s, 100 systolic is very reasonable blood pressure, and it does not concern us. In fact, that's one of the places we want to go. We'd also encourage you to treat the patient and not the creatinine. 

Many times we'll see the creatinine bump with an institution of an ACE inhibitor, and patients will be providers will tend to pull back. We typically tolerate at least a 30% rise in the creatinine and oftentimes if the creatinine does rise, we will hold and just recheck the labs in a couple of weeks. 

One of the other things that I've found that is really helpful in getting people to buy into these medicines is using something called the Seattle Heart Failure Model, as referenced in this slide. 


This Seattle Heart Failure Model is a tool that's free for all people to use. You just Google: the Seattle heart failure model, and in it, you can put in characteristics about your patient, their ejection fraction, their age, their sodium, a bunch of factors about them. And it will spit out a number that suggests what is their mean life expectancy. I don't do this as you did turn to the patient and say this is how long you have to live. 

There's a huge variation in that. And we don't know how long patients are going to live. And they love to prove us wrong as you know. But this is an average, so if you take someone with your ejection fraction, with your labs, with your age, on these therapies on average, this is how long patients live for about. 

And then what you can do with this model is show them that if you add in an ACE inhibitor, if you add in a beta-blocker, if you add in spironolactone, if you add an implantable cardiac defibrillator – what does that do to the average life expectancy? 

And it will typically more than double that. That can go a long way when patients aren't quite sure if they feel a little bit fatigued on metoprolol want to wonder if they should stay on it. Once they learn that their average life expectancy more than doubles. Oftentimes, I find that patients have a greater interest in moving forward with this. 


Let's go back to our patient, the initial question that we started with. We had a 48-year-old man with an E.F. of 28% non-ischemic cardiomyopathy. Pretty minimal symptoms. He was on atenolol, lisinopril, and furosemide. So the blood pressure is 122 over 76, heart rate 68, his kidney function and potassium. 

So, what is the next most appropriate change to his medical therapy? It should be started with sacubitril/valsartan titrated atenolol to a goal of 100; transition atenolol to metoprolol succinate and titrate lisinopril start spironolactone or no change in therapy. 

And here I would argue that the best answer is to titrate atenolol, which is not on the list of the preferred beta-blockers to metoprolol succinate, and metoprolol succinate is on the list of the three preferred beta-blockers and then to titrate to goal dose. 

You could make an argument to titrate lisinopril up further, but 20 milligrams is a reasonable dose of that. 


Alright, so we made it through our first two objectives. And now we're going to talk a little bit about, when do you add on further therapies beyond the ACE inhibitor and beta-blockers such as spironolactone or a drug called a neprilysin inhibitor. So we'll go back to our patient again. 

He has an ejection fraction again of 28%. But now he's on metoprolol succinate 200 milligrams daily. He's otherwise doing well. He's on lisinopril. He's on a diuretic, potassium and kidney function are doing fine. And what is the next best step for him? And so should you transition lisinopril to sacubitril/valsartan, transition metoprolol succinate need to carvedilol, start spironolactone, or refer for a cardiac resynchronization device. 

And I would argue here that the best answer is probably to start spironolactone, and we'll go through that. The other option would be the neprilysin inhibitor. So we're going back to our foundations of heart failure management. Again, if they're volume overloaded, treat them with loop diuretics, once they're euvolemic and stable, then add on an ACE inhibitor and a beta-blocker and titrate those to the goal or maximally tolerated dosages. 


The next step in select groups. And you can do one or both of these, and this is what the question was getting at would be to add spironolactone, or to replace the ACE or ARB with a drug that is the neprilysin inhibitor, which is called sacubitril/valsartan So let's talk for a minute about an aldosterone antagonist, so potassium-sparing diuretic, neural hormonal antagonist. And here's a prominent trial called the RALES trial. In this trial, they randomized patients with heart failure with reduced ejection fraction to spironolactone versus placebo. 

After about three years, there was an 11% absolute risk reduction in mortality, which is a substantial risk reduction with our medical therapies. 

If we start to look at what's the combined effect of medical therapy, where we're looking back again at our patient who has a baseline survival of one year. If their baseline survival is one year, you can see in the light blue and the slide where you add on an ACE inhibitor, you see in the orange where you add on a beta-blocker. 


And then, finally, with the aldosterone antagonists, you get even more life expectancy on average. The number needed to treat to prevent one death over three years with spironolactone using multiple different studies, the average is felt to be approximately 6. 

That's even better than beta-blockers or ACE inhibitors. However, as we look at the number of patients who are actually on this therapy, who should receive it. This is even worse than ACE inhibitors and beta-blockers. Only about a third of patients, who have heart failure reduced ejection fraction, are on spironolactone. Now, the medication is a bit easier to titrate because typically we'll start with 25 milligrams, and stay there or start with 12.5 and go to 25. So more, more of the patients are at target dosages. 


So, some practical tips on how to use aldosterone antagonists. Typically, we will use these in patients who have reasonably normal renal function. Once the creatine gets above 2 and women are more than 2.5 in men, then we typically hold off. We also watch the potassium very closely.

We do not initiate if the potassium is greater than 5. And if they're already on the medicine and as long as the potassium is less than 5.5, we'll hold the course if we find that there are problems with hyperkalemia, it's making sure that they are not on any potassium supplementation and also thinking about a low potassium diet. 

We typically start spironolactone, which is generic. There is another drug called eplerenone,  which has similar outcomes. The one benefit over eplerenone is that eplerenone does not cause gynecomastia or breast tenderness, which occurs in about 10% of patients who take spironolactone. Spironolactone is our first choice unless we get to gynecomastia and then we'll try eplerenone, eplerenone as much more expensive. 

We are relatively vigorous with checking potassium. I think is the biggest risk with this drug is causing hyperkalemia. I'll often check potassium at two weeks, at three months, and then at least once, if not twice a year, depending on how their potassium has looked after them. 


So the other option is selected groups after they've already been on the ACE inhibitor and beta-blocker is to think once the first option was to think about spironolactone and the second one be to replace the ACE or ARB with a drug called sacubitril/valsartan. 

Sacubitril/valsartan is a drug called an ARNI. And what's an Arni? An ARNI is an angiotensin receptor blocker and neprilysin inhibitor, so it's actually two drugs. Sacubitril is one of the drugs. Valsartan is the other drug. And the way that sacubitril works, and I think we're familiar with valsartan as an angiotensin receptor blocker, but the additive thing here is this sacubitril. 

So, the way that sacubitril works is that it affects the levels of BNP in the body, so when your heart is under stretch or strain, it gives off something called pro-BNP. pro-BNP is cleaved into NT-proBNP, which is biologically inactive, and BNP, which is biologically active. Now BNP is helpful. So BNP decreases neurohormonal activation. BNP promotes vasodilation, which is what we want when patients have heart failure. BNP reduces cardiac fibrosis hypertrophy and also helps with diuresis. It's a mild natriuretic. 

Those are all things that we like and there is a substance called neprilysin, and neprilysin takes BNP, which is working in someone's body, and it breaks it down into inactive metabolites. And sacubitril is the drug that we have that inhibits the breakdown of BNP by inhibiting neprilysin. So basically sacubitril allows biologically active BNP to stick around for longer and to have more of it available. 


There is a large double-blind placebo-controlled trial, which has looked at this medication. It's called the Paradigm, the Paradigm Heart Failure Study. And in this study, there was a reduction in all-cause mortality and it was about a 2.8% absolute risk reduction over about 27 months. The number of heart failure hospitalizations, there was about a 3% absolute risk reduction over the same time period. 

So, if we look at the number needed to treat to save one life and we've talked about ACE inhibitors, which has a number needed to treat of about 26: beta-blockers 9, spironolactone or aldosterone antagonist 6. Sacubitril/valsartan has a number needed to treat of about 15. If someone is not already on an ACE or angiotensin receptor blocker, the number needed to treat of about 29 when it's incremental to an ACE inhibitor. 

So, another question for you here is what would be the most common adverse reaction after starting sacubitril/valsartan? 

A. renal failure, 

B. symptomatic hypertension, 

C. hyperkalemia, 

D. headaches, 

E. angioedema? 

(answer below)

And the answer here is symptomatic hypotension. So, the addition of sacubitril to valsartan tends to cause more vigorous hypotension, and we typically will not start if the systolic blood pressure is less than about 100 mmHg. Some practical tips when starting this drug are that I would stick with the trial entry criteria. The ejection fraction should be less than 40%, despite patients already being on goal-directed medical therapy. 

New York Heart Association class 2 to 3 patients. And one of the important things that have come out with a trial and with studying this drug is that it is important to stop the ACE inhibitor about 36 hours prior. 

There have been reports of angioedema, also just reports of increased side effects when you have an ACE inhibitor. Then you add on valsartan and sacubitril all at the same time. The primary reason is to avoid rare cases of angioedema. And you may need to back off on the diuretic because this sacubitril does have some diuretic effects. 


So, one of the questions is: should we spironolactone or sacubitril/valsartan, or both? And there are some variables, I think, that should take into account here. If the blood pressure is low, then generally will avoid sacubitril. If there's hyperkalemia, we'll avoid spironolactone. I think one of the things that we don't often talk about is heart failure in medicine in general enough. It also is cost. 

If you look at the yearly cost of these drugs, ACE inhibitors, beta-blockers, spironolactone, those are all generic drugs that have been around for years. The cost of one year of an ACE inhibitor, a beta-blocker or spironolactone, is probably about $48 a year. These are often sacubitril/valsartan because it is new and the patent is roughly $5,000 a year. If you were to pay the full price out of pocket. Now many drug companies are supporting this drug, but the costs are substantial. 


Here's one approach to medical management that sums up so far what we've talked about with heart failure with reduced ejection fraction. Step one, if a patient comes to you and they have heart-reduced ejection fraction and their volume overloaded, they need to be treated with a loop diuretic. 

Step two, once they are euvolemic and stable, then they should be put on an ACE inhibitor and a beta-blocker and those should be titrated to the goal or maximally tolerated dosages

Step three, if the potassium and creatinine are acceptable, then I encourage you to start the spironolactone number needed to treat 6 to save a life. 

Step four, if blood pressure and cost are acceptable, then it is reasonable to replace the ACE or ARB with sacubitril/valsartan. Now, we're gonna get to our last objective. And I think it's just a practical thing about when and if the systolic function improves. How long does treatment need to be continued and what can be stopped? This is a question I'll often see in patients who have had heart failure and they come back in their ejection fraction is better. 


So we'll take a 49-year-old man as an example. And now his ejection fraction has improved. Let's say it's our patient. It's a year later. He used to be 48, now he's 49; his E.F. is now 55%. He has no symptoms. He's on metoprolol 200 a day, lisinopril 20 milligrams daily, spironolactone 25 milligrams daily. You've done an excellent job up-titrating – his medications, blood pressure, and heart rate are reasonable. Potassium and kidney function are okay too. 

And he says can I stop any of these medications? You could wean the furosemide, we lisinopril, wean metoprolol, stop spironolactone, or hold the course. So several different options. And when I get this question, can I stop my heart failure medicines? 


In general, I tell patients that it's reasonable to wean the diuretics if they're euvolemic and stable and doing well. If patients find that when they wean off the diuretics, they're filling back up with fluid, becoming more short of breath, their weight is going back up, then you need to get back on the diuretics. There should be some ability of that patient to monitor themselves at that point. 

So if not tolerated, go back to the previous effective dose. There is one small trial and limited data to try to guide us over what are the risks of medication withdrawal in patients, who have withdrawn medications. This is a small trial and a patient, a group of patients who had idiopathic dilated cardiomyopathy, and they had two groups. One group continued their medications, and when they looked at the number of events over the next 6 months, there were no events in that group, so no heart failure events. 

And they had metrics such as did the NT-proBNP double? Were they hospitalized? Were there clinical signs of heart failure that recurred? And this is compared to the treatment withdrawal group where about 40% or nearly half of the patients had some worsening at 6 months when you withdrew their therapy. 

If patients ask, can I stop my heart failure medications, I'd say that many patients deemed to have recovered can relapse? And this is from an idiopathic dilated cardiomyopathy, and they would relapse following treatment withdrawal. 

Until robust predictors of relapse are identified, we think that treatment should continue indefinitely. So the answer to our question is, can I stop my heart failure meds? It'd be reasonable to wean the furosemide or to hold the course


So, heart failure, in general, it's a clinical diagnosis. There's no one test that's going to tell you whether if there's heart failure, you need to be bringing multiple data points together. 

History, physical exam, and laboratory testing are trying to make that diagnosis. An ECHO is critical and helps you understand both why there is heart failure, but also how to treat patients who have heart failure. The treatment of heart failure with reduced ejection fraction is markedly different than heart failure with preserved ejection fraction. 

Second main point is that medical therapy works, but it's underutilized. And this is in patients with heart failure with reduced ejection fraction, remembering that that patient needs to be put on that ACE inhibitor or angiotensin receptor blocker, a heart failure specific beta-blocker, and those should be up titrated to the maximum tolerated or goal-directed dosages. 

Dosages that were used in clinical trials; aldosterone antagonists are something that you should not forget. It's also very underutilized. The number needed to treat here to save a life is 6. With the recovery of ejection fraction, it's OK to stop the diuretics. But neurohormonal antagonists should be continued lifelong.

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