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REALIZE-K: A New Potassium Binder to Help Keep Spiro on Board
This transcript has been edited for clarity.
We have talked often in the past about potassium. Why is potassium so important in heart failure? It’s because many doctors are afraid to give some of the drugs that will raise the potassium, because then you need to deal with it —and everybody is afraid of hyperkalemia causing arrhythmias.
Calm those nerves. Just remember that arrhythmias only occur when the potassium suddenly goes up. This chronic hyperkalemia, which occurs with many of our drugs, usually — I can’t say every time — does not result in arrhythmias.
Patiromer and Zirconium Cyclosilicate
Now, we’ve got potassium binders. You’ve heard me talk about the potassium binders in several of my other chats with you, and they work. We have primarily two of them. The first one that came out was patiromer, and now I’m going to talk to you a little bit about zirconium cyclosilicate, which uses sodium as its exchange ion. Whenever you take out one ion, you have to put another one in, and in this case it’s sodium. Maybe if you use it in the higher doses, you can give the patient more edema or you can make the patient congested with more fluid.
Years ago we did the DIAMOND study; it was a patiromer study, but in essence we found that you could continue to give the drug, particularly the mineralocorticoid receptor antagonists (MRAs) such as spironolactone or eplerenone, as long as you have the patiromer as your safety net, and that the drugs were well tolerated and the adverse events were significantly less.
The REALIZE-K Trial
Now, let’s talk about the REALIZE-K trial. The researchers wanted to prove basically the same thing: that the patients could be started or kept on their spironolactone as long as you had that backup of the zirconium cyclosilicate binder.
They picked patients who had HFrEF — so, low ejection fractions, defined as less than 40% — and they were already on guideline-directed medical therapy, but not an MRA. They divided up the patients right from the beginning between those who were already hyperkalemic — in other words, they had potassiums of 5.1-5.9 mEq/L, which is when doctors start getting worried. GFRs had to be better than 30 mL/min per 1.73 m2, and if the potassium was not yet okay, they were given the zirconium cyclosilicate to normalize the potassium and then they entered the study.
The second group had some history of or were at risk for hyperkalemia. Maybe their GFRs were lower, but their potassiums were somewhere between 3.5 and 5 mEq/L.
They started with about 366 patients. These trials have not been huge, certainly not what we normally see in heart failure trials. About 95 patients had hyperkalemia initially and 271 patients were normokalemic.
Then they were randomized; about 102 patients went on the potassium binder and the other group went on the placebo. They continued the study and they continued to check whether the patient had to come off the drug or had to reduce or remove the spironolactone.
These were older patients, mostly in their early seventies. This was an international trial. There were not that many patients from North America, but they had quite a few patients from Europe and some patients from Latin America. There were many with diabetes, atrial fibrillation, and all the usual comorbidities that we typically see.
The proportions of patients classified as New York Heart Association Class III and IV were about 16% to 17% and the rest were Class II, so this is really the ambulatory population. NT-proBNP levels were elevated, at approximately 1000-1200 pg/mL, and the GFRs were either in the high 40s or about 60 mL/min per 1.73 m2. The patients were pretty well medicated, including with RAAS inhibition, beta-blockers, and even SGLT2 inhibitors.
This is a very typical population and they wanted to see what happened. Did the patients remain on the binder and were they able to tolerate the spironolactone? In fact, that was the case.
At the end of the study, more patients had been able to stay on their spironolactone, which is that one drug that we’re not doing so well on when you look at large databases. If they were on the zirconium drug, they were more likely to stay on the spironolactone. They even did a sensitivity analysis, which really showed that it was consistent across the board.
Edema and Hyperkalemia
Now we have two binders that have shown to us that patients can stay on their drugs. There were some interesting findings here, though.
There was more edema — again, everything is based on small numbers — and there seemed to be more heart failure events in the group that received the zirconium cyclosilicate. The first episode of hyperkalemia was delayed or didn’t happen at all. Again, the hyperkalemia was controlled.
What does that tell you? Well, the exchange is sodium. There had been reports before that if you gave this binder at the higher doses, you would have more retention of sodium. I think we see that in this trial, even though the numbers are very small.
According to the investigators, these were issues that could be resolved through an increase in diuretics or having the patient remember to be careful with their sodium intake so they don’t retain more fluid.
My message to you is to use these binders, whichever one of the two you want or whichever your hospital has available for you on their formulary, because it may give you that sense of comfort and self-efficacy so that you can actually start your patients on an MRA and keep them on it.
The MRAs are lifesaving drugs and the patients with HFrEF need to be on them. This is a way to do it without having to sacrifice your true guideline-directed medical therapy.
Dr. Piña, Professor of Medicine/Cardiology/Heart Failure/Transplant; Quality Officer, Cardiovascular Line, Sidney Kimmel College of Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania; Clinical Professor of Medicine, Central Michigan University College of Medicine, Mount Pleasant, Michigan; Adjunct Professor of Epidemiology and Biostatistics, Population & Quantitative Health Sciences, Case Western University, Cleveland, Ohio, disclosed ties with the Food and Drug Administration’s Center for Devices and Radiological Health.
A version of this article appeared on Medscape.com
This transcript has been edited for clarity.
We have talked often in the past about potassium. Why is potassium so important in heart failure? It’s because many doctors are afraid to give some of the drugs that will raise the potassium, because then you need to deal with it —and everybody is afraid of hyperkalemia causing arrhythmias.
Calm those nerves. Just remember that arrhythmias only occur when the potassium suddenly goes up. This chronic hyperkalemia, which occurs with many of our drugs, usually — I can’t say every time — does not result in arrhythmias.
Patiromer and Zirconium Cyclosilicate
Now, we’ve got potassium binders. You’ve heard me talk about the potassium binders in several of my other chats with you, and they work. We have primarily two of them. The first one that came out was patiromer, and now I’m going to talk to you a little bit about zirconium cyclosilicate, which uses sodium as its exchange ion. Whenever you take out one ion, you have to put another one in, and in this case it’s sodium. Maybe if you use it in the higher doses, you can give the patient more edema or you can make the patient congested with more fluid.
Years ago we did the DIAMOND study; it was a patiromer study, but in essence we found that you could continue to give the drug, particularly the mineralocorticoid receptor antagonists (MRAs) such as spironolactone or eplerenone, as long as you have the patiromer as your safety net, and that the drugs were well tolerated and the adverse events were significantly less.
The REALIZE-K Trial
Now, let’s talk about the REALIZE-K trial. The researchers wanted to prove basically the same thing: that the patients could be started or kept on their spironolactone as long as you had that backup of the zirconium cyclosilicate binder.
They picked patients who had HFrEF — so, low ejection fractions, defined as less than 40% — and they were already on guideline-directed medical therapy, but not an MRA. They divided up the patients right from the beginning between those who were already hyperkalemic — in other words, they had potassiums of 5.1-5.9 mEq/L, which is when doctors start getting worried. GFRs had to be better than 30 mL/min per 1.73 m2, and if the potassium was not yet okay, they were given the zirconium cyclosilicate to normalize the potassium and then they entered the study.
The second group had some history of or were at risk for hyperkalemia. Maybe their GFRs were lower, but their potassiums were somewhere between 3.5 and 5 mEq/L.
They started with about 366 patients. These trials have not been huge, certainly not what we normally see in heart failure trials. About 95 patients had hyperkalemia initially and 271 patients were normokalemic.
Then they were randomized; about 102 patients went on the potassium binder and the other group went on the placebo. They continued the study and they continued to check whether the patient had to come off the drug or had to reduce or remove the spironolactone.
These were older patients, mostly in their early seventies. This was an international trial. There were not that many patients from North America, but they had quite a few patients from Europe and some patients from Latin America. There were many with diabetes, atrial fibrillation, and all the usual comorbidities that we typically see.
The proportions of patients classified as New York Heart Association Class III and IV were about 16% to 17% and the rest were Class II, so this is really the ambulatory population. NT-proBNP levels were elevated, at approximately 1000-1200 pg/mL, and the GFRs were either in the high 40s or about 60 mL/min per 1.73 m2. The patients were pretty well medicated, including with RAAS inhibition, beta-blockers, and even SGLT2 inhibitors.
This is a very typical population and they wanted to see what happened. Did the patients remain on the binder and were they able to tolerate the spironolactone? In fact, that was the case.
At the end of the study, more patients had been able to stay on their spironolactone, which is that one drug that we’re not doing so well on when you look at large databases. If they were on the zirconium drug, they were more likely to stay on the spironolactone. They even did a sensitivity analysis, which really showed that it was consistent across the board.
Edema and Hyperkalemia
Now we have two binders that have shown to us that patients can stay on their drugs. There were some interesting findings here, though.
There was more edema — again, everything is based on small numbers — and there seemed to be more heart failure events in the group that received the zirconium cyclosilicate. The first episode of hyperkalemia was delayed or didn’t happen at all. Again, the hyperkalemia was controlled.
What does that tell you? Well, the exchange is sodium. There had been reports before that if you gave this binder at the higher doses, you would have more retention of sodium. I think we see that in this trial, even though the numbers are very small.
According to the investigators, these were issues that could be resolved through an increase in diuretics or having the patient remember to be careful with their sodium intake so they don’t retain more fluid.
My message to you is to use these binders, whichever one of the two you want or whichever your hospital has available for you on their formulary, because it may give you that sense of comfort and self-efficacy so that you can actually start your patients on an MRA and keep them on it.
The MRAs are lifesaving drugs and the patients with HFrEF need to be on them. This is a way to do it without having to sacrifice your true guideline-directed medical therapy.
Dr. Piña, Professor of Medicine/Cardiology/Heart Failure/Transplant; Quality Officer, Cardiovascular Line, Sidney Kimmel College of Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania; Clinical Professor of Medicine, Central Michigan University College of Medicine, Mount Pleasant, Michigan; Adjunct Professor of Epidemiology and Biostatistics, Population & Quantitative Health Sciences, Case Western University, Cleveland, Ohio, disclosed ties with the Food and Drug Administration’s Center for Devices and Radiological Health.
A version of this article appeared on Medscape.com
This transcript has been edited for clarity.
We have talked often in the past about potassium. Why is potassium so important in heart failure? It’s because many doctors are afraid to give some of the drugs that will raise the potassium, because then you need to deal with it —and everybody is afraid of hyperkalemia causing arrhythmias.
Calm those nerves. Just remember that arrhythmias only occur when the potassium suddenly goes up. This chronic hyperkalemia, which occurs with many of our drugs, usually — I can’t say every time — does not result in arrhythmias.
Patiromer and Zirconium Cyclosilicate
Now, we’ve got potassium binders. You’ve heard me talk about the potassium binders in several of my other chats with you, and they work. We have primarily two of them. The first one that came out was patiromer, and now I’m going to talk to you a little bit about zirconium cyclosilicate, which uses sodium as its exchange ion. Whenever you take out one ion, you have to put another one in, and in this case it’s sodium. Maybe if you use it in the higher doses, you can give the patient more edema or you can make the patient congested with more fluid.
Years ago we did the DIAMOND study; it was a patiromer study, but in essence we found that you could continue to give the drug, particularly the mineralocorticoid receptor antagonists (MRAs) such as spironolactone or eplerenone, as long as you have the patiromer as your safety net, and that the drugs were well tolerated and the adverse events were significantly less.
The REALIZE-K Trial
Now, let’s talk about the REALIZE-K trial. The researchers wanted to prove basically the same thing: that the patients could be started or kept on their spironolactone as long as you had that backup of the zirconium cyclosilicate binder.
They picked patients who had HFrEF — so, low ejection fractions, defined as less than 40% — and they were already on guideline-directed medical therapy, but not an MRA. They divided up the patients right from the beginning between those who were already hyperkalemic — in other words, they had potassiums of 5.1-5.9 mEq/L, which is when doctors start getting worried. GFRs had to be better than 30 mL/min per 1.73 m2, and if the potassium was not yet okay, they were given the zirconium cyclosilicate to normalize the potassium and then they entered the study.
The second group had some history of or were at risk for hyperkalemia. Maybe their GFRs were lower, but their potassiums were somewhere between 3.5 and 5 mEq/L.
They started with about 366 patients. These trials have not been huge, certainly not what we normally see in heart failure trials. About 95 patients had hyperkalemia initially and 271 patients were normokalemic.
Then they were randomized; about 102 patients went on the potassium binder and the other group went on the placebo. They continued the study and they continued to check whether the patient had to come off the drug or had to reduce or remove the spironolactone.
These were older patients, mostly in their early seventies. This was an international trial. There were not that many patients from North America, but they had quite a few patients from Europe and some patients from Latin America. There were many with diabetes, atrial fibrillation, and all the usual comorbidities that we typically see.
The proportions of patients classified as New York Heart Association Class III and IV were about 16% to 17% and the rest were Class II, so this is really the ambulatory population. NT-proBNP levels were elevated, at approximately 1000-1200 pg/mL, and the GFRs were either in the high 40s or about 60 mL/min per 1.73 m2. The patients were pretty well medicated, including with RAAS inhibition, beta-blockers, and even SGLT2 inhibitors.
This is a very typical population and they wanted to see what happened. Did the patients remain on the binder and were they able to tolerate the spironolactone? In fact, that was the case.
At the end of the study, more patients had been able to stay on their spironolactone, which is that one drug that we’re not doing so well on when you look at large databases. If they were on the zirconium drug, they were more likely to stay on the spironolactone. They even did a sensitivity analysis, which really showed that it was consistent across the board.
Edema and Hyperkalemia
Now we have two binders that have shown to us that patients can stay on their drugs. There were some interesting findings here, though.
There was more edema — again, everything is based on small numbers — and there seemed to be more heart failure events in the group that received the zirconium cyclosilicate. The first episode of hyperkalemia was delayed or didn’t happen at all. Again, the hyperkalemia was controlled.
What does that tell you? Well, the exchange is sodium. There had been reports before that if you gave this binder at the higher doses, you would have more retention of sodium. I think we see that in this trial, even though the numbers are very small.
According to the investigators, these were issues that could be resolved through an increase in diuretics or having the patient remember to be careful with their sodium intake so they don’t retain more fluid.
My message to you is to use these binders, whichever one of the two you want or whichever your hospital has available for you on their formulary, because it may give you that sense of comfort and self-efficacy so that you can actually start your patients on an MRA and keep them on it.
The MRAs are lifesaving drugs and the patients with HFrEF need to be on them. This is a way to do it without having to sacrifice your true guideline-directed medical therapy.
Dr. Piña, Professor of Medicine/Cardiology/Heart Failure/Transplant; Quality Officer, Cardiovascular Line, Sidney Kimmel College of Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania; Clinical Professor of Medicine, Central Michigan University College of Medicine, Mount Pleasant, Michigan; Adjunct Professor of Epidemiology and Biostatistics, Population & Quantitative Health Sciences, Case Western University, Cleveland, Ohio, disclosed ties with the Food and Drug Administration’s Center for Devices and Radiological Health.
A version of this article appeared on Medscape.com
Heart failure guidelines update: What the ESC got right
This transcript has been edited for clarity.
This is my usual blog, except I am here from the absolutely beautiful city of Amsterdam, where the annual congress of the European Society of Cardiology has been going on.
SGLT2 inhibitors for HFpEF and HFrEF
I’m going to review very briefly the 2023 focused update to the ESC heart failure guidelines. Theresa McDonagh was the first author of this and of the previous ESC or European guidelines. These are a little bit different than the American guidelines, which were presented in 2022. We know that we need an update. The Europeans have gotten ahead of us, and now we have the European update, which I find incredibly well written and it really highlights the areas that I think the takeaways are for the clinicians.
First, we have been seeing now for several years – since 2018 – the benefits of the sodium-glucose cotransporter 2 (SGLT2) inhibitors. Every time we lift the veil on something, there they are in a positive light. We have learned about heart failure with reduced ejection fraction (HFrEF) for both empagliflozin and dapagliflozin. There are very similar results. One population may be enriched with a little of this and a little of that, but the basic messages are the same. In HFrEF, both of these drugs improve outcomes and it happens quickly. You don’t have to wait 1 or 2 years to see this. Within months, and actually within days, you start to see the curves split apart statistically.
The next logical ground was heart failure with preserved ejection fraction (HFpEF). The definition, when we started the HFpEF trials, was 45% or greater. I want the audience to realize that, in the midst of all these trials, we came out – we meaning the American Heart Association, the American College of Cardiology, and the Heart Failure Society – with the new definition of heart failure, which said that true HFpEF is 50% or greater. That in-between zone of 40%-50% or 41%-49% is mRF, or mid-range, what I call middle of the road. I think the Europeans have really emphasized that to us. I believe that those patients really behave much more like a HFrEF population.
Now that we have very positive findings with the SGLT2 inhibitors, both dapagliflozin and empagliflozin, in HFpEF – defined, as I said, as 40% or 45% or greater, not necessarily 50% – with excellent point estimates that just line up, one on top of the other. It doesn’t matter if patients have diabetes or not; the results are exactly the same.
This has been so promising that I am not surprised that the Europeans elevated the SGLT2 inhibitors to a class 1A indication. In the United States in 2022, we thought we were really way ahead by calling it a class 2A indication. Well, now it’s a class 1A indication in Europe, and I have a feeling that the AHA and the ACC are going to start talking about an update because the data are so strong.
Now, we even have data on initiating these drugs in the hospital. EMPULSE was a very large trial about the benefits of starting these drugs in the hospital. You do not have to wait until the patient is in the outpatient setting. You can start it in the hospital.
When? I have no specific day that I start it. I used to try to do a good diuresis first, get the patients somewhat decongested, and then start it. I don’t want to deprive the patients of the benefits of these drugs that happen very early by waiting until the patients are in the outpatient setting.
In the United States, we’ve had some issues with coverage of some of these drugs. In my institution, we now have both on the formulary, and I pick the drug depending upon the patient’s coverage. Medicare pretty much covers most of them. If the patient is older but not yet a Medicare patient, they may have a very large copay. I advise you to get your offices or your health system to look into this so that, when you give the prescription to the patient, whether they’re leaving the hospital or are now in your clinics, they can actually get the drug.
Finerenone and intravenous iron
There is an additional recommendation in these guidelines for finerenone, the mineralocorticoid receptor agonist that I’ve discussed before, that has some really promising data on type 2 diabetes with chronic kidney disease. They have called that a class 1A indication for finerenone. I think there is more to come.
One more: the iron deficiency. Giving intravenous iron actually does improve symptoms and quality of life. I have seen this in my own patients, so I have been very diligent at looking for iron deficiency.
It is a new era. We have more tools, obviously, for our patients. It means one more drug, and that’s always a challenge. We’ve already been doing the pillars of care. This is the fourth pillar of care, but now with a class 1A indication.
Take a look. They’re easy to read. Dr. McDonagh is the first author, and I think they’ve been extremely well done.
Dr. Piña is professor of medicine at Thomas Jefferson University Hospital in Philadelphia. She is a heart failure and cardiac transplantation expert. She disclosed serving as an adviser/consultant to the FDA’s Center for Devices and Radiological Health and has been a volunteer for the American Heart Association since 1982.
A version of this article appeared on Medscape.com.
This transcript has been edited for clarity.
This is my usual blog, except I am here from the absolutely beautiful city of Amsterdam, where the annual congress of the European Society of Cardiology has been going on.
SGLT2 inhibitors for HFpEF and HFrEF
I’m going to review very briefly the 2023 focused update to the ESC heart failure guidelines. Theresa McDonagh was the first author of this and of the previous ESC or European guidelines. These are a little bit different than the American guidelines, which were presented in 2022. We know that we need an update. The Europeans have gotten ahead of us, and now we have the European update, which I find incredibly well written and it really highlights the areas that I think the takeaways are for the clinicians.
First, we have been seeing now for several years – since 2018 – the benefits of the sodium-glucose cotransporter 2 (SGLT2) inhibitors. Every time we lift the veil on something, there they are in a positive light. We have learned about heart failure with reduced ejection fraction (HFrEF) for both empagliflozin and dapagliflozin. There are very similar results. One population may be enriched with a little of this and a little of that, but the basic messages are the same. In HFrEF, both of these drugs improve outcomes and it happens quickly. You don’t have to wait 1 or 2 years to see this. Within months, and actually within days, you start to see the curves split apart statistically.
The next logical ground was heart failure with preserved ejection fraction (HFpEF). The definition, when we started the HFpEF trials, was 45% or greater. I want the audience to realize that, in the midst of all these trials, we came out – we meaning the American Heart Association, the American College of Cardiology, and the Heart Failure Society – with the new definition of heart failure, which said that true HFpEF is 50% or greater. That in-between zone of 40%-50% or 41%-49% is mRF, or mid-range, what I call middle of the road. I think the Europeans have really emphasized that to us. I believe that those patients really behave much more like a HFrEF population.
Now that we have very positive findings with the SGLT2 inhibitors, both dapagliflozin and empagliflozin, in HFpEF – defined, as I said, as 40% or 45% or greater, not necessarily 50% – with excellent point estimates that just line up, one on top of the other. It doesn’t matter if patients have diabetes or not; the results are exactly the same.
This has been so promising that I am not surprised that the Europeans elevated the SGLT2 inhibitors to a class 1A indication. In the United States in 2022, we thought we were really way ahead by calling it a class 2A indication. Well, now it’s a class 1A indication in Europe, and I have a feeling that the AHA and the ACC are going to start talking about an update because the data are so strong.
Now, we even have data on initiating these drugs in the hospital. EMPULSE was a very large trial about the benefits of starting these drugs in the hospital. You do not have to wait until the patient is in the outpatient setting. You can start it in the hospital.
When? I have no specific day that I start it. I used to try to do a good diuresis first, get the patients somewhat decongested, and then start it. I don’t want to deprive the patients of the benefits of these drugs that happen very early by waiting until the patients are in the outpatient setting.
In the United States, we’ve had some issues with coverage of some of these drugs. In my institution, we now have both on the formulary, and I pick the drug depending upon the patient’s coverage. Medicare pretty much covers most of them. If the patient is older but not yet a Medicare patient, they may have a very large copay. I advise you to get your offices or your health system to look into this so that, when you give the prescription to the patient, whether they’re leaving the hospital or are now in your clinics, they can actually get the drug.
Finerenone and intravenous iron
There is an additional recommendation in these guidelines for finerenone, the mineralocorticoid receptor agonist that I’ve discussed before, that has some really promising data on type 2 diabetes with chronic kidney disease. They have called that a class 1A indication for finerenone. I think there is more to come.
One more: the iron deficiency. Giving intravenous iron actually does improve symptoms and quality of life. I have seen this in my own patients, so I have been very diligent at looking for iron deficiency.
It is a new era. We have more tools, obviously, for our patients. It means one more drug, and that’s always a challenge. We’ve already been doing the pillars of care. This is the fourth pillar of care, but now with a class 1A indication.
Take a look. They’re easy to read. Dr. McDonagh is the first author, and I think they’ve been extremely well done.
Dr. Piña is professor of medicine at Thomas Jefferson University Hospital in Philadelphia. She is a heart failure and cardiac transplantation expert. She disclosed serving as an adviser/consultant to the FDA’s Center for Devices and Radiological Health and has been a volunteer for the American Heart Association since 1982.
A version of this article appeared on Medscape.com.
This transcript has been edited for clarity.
This is my usual blog, except I am here from the absolutely beautiful city of Amsterdam, where the annual congress of the European Society of Cardiology has been going on.
SGLT2 inhibitors for HFpEF and HFrEF
I’m going to review very briefly the 2023 focused update to the ESC heart failure guidelines. Theresa McDonagh was the first author of this and of the previous ESC or European guidelines. These are a little bit different than the American guidelines, which were presented in 2022. We know that we need an update. The Europeans have gotten ahead of us, and now we have the European update, which I find incredibly well written and it really highlights the areas that I think the takeaways are for the clinicians.
First, we have been seeing now for several years – since 2018 – the benefits of the sodium-glucose cotransporter 2 (SGLT2) inhibitors. Every time we lift the veil on something, there they are in a positive light. We have learned about heart failure with reduced ejection fraction (HFrEF) for both empagliflozin and dapagliflozin. There are very similar results. One population may be enriched with a little of this and a little of that, but the basic messages are the same. In HFrEF, both of these drugs improve outcomes and it happens quickly. You don’t have to wait 1 or 2 years to see this. Within months, and actually within days, you start to see the curves split apart statistically.
The next logical ground was heart failure with preserved ejection fraction (HFpEF). The definition, when we started the HFpEF trials, was 45% or greater. I want the audience to realize that, in the midst of all these trials, we came out – we meaning the American Heart Association, the American College of Cardiology, and the Heart Failure Society – with the new definition of heart failure, which said that true HFpEF is 50% or greater. That in-between zone of 40%-50% or 41%-49% is mRF, or mid-range, what I call middle of the road. I think the Europeans have really emphasized that to us. I believe that those patients really behave much more like a HFrEF population.
Now that we have very positive findings with the SGLT2 inhibitors, both dapagliflozin and empagliflozin, in HFpEF – defined, as I said, as 40% or 45% or greater, not necessarily 50% – with excellent point estimates that just line up, one on top of the other. It doesn’t matter if patients have diabetes or not; the results are exactly the same.
This has been so promising that I am not surprised that the Europeans elevated the SGLT2 inhibitors to a class 1A indication. In the United States in 2022, we thought we were really way ahead by calling it a class 2A indication. Well, now it’s a class 1A indication in Europe, and I have a feeling that the AHA and the ACC are going to start talking about an update because the data are so strong.
Now, we even have data on initiating these drugs in the hospital. EMPULSE was a very large trial about the benefits of starting these drugs in the hospital. You do not have to wait until the patient is in the outpatient setting. You can start it in the hospital.
When? I have no specific day that I start it. I used to try to do a good diuresis first, get the patients somewhat decongested, and then start it. I don’t want to deprive the patients of the benefits of these drugs that happen very early by waiting until the patients are in the outpatient setting.
In the United States, we’ve had some issues with coverage of some of these drugs. In my institution, we now have both on the formulary, and I pick the drug depending upon the patient’s coverage. Medicare pretty much covers most of them. If the patient is older but not yet a Medicare patient, they may have a very large copay. I advise you to get your offices or your health system to look into this so that, when you give the prescription to the patient, whether they’re leaving the hospital or are now in your clinics, they can actually get the drug.
Finerenone and intravenous iron
There is an additional recommendation in these guidelines for finerenone, the mineralocorticoid receptor agonist that I’ve discussed before, that has some really promising data on type 2 diabetes with chronic kidney disease. They have called that a class 1A indication for finerenone. I think there is more to come.
One more: the iron deficiency. Giving intravenous iron actually does improve symptoms and quality of life. I have seen this in my own patients, so I have been very diligent at looking for iron deficiency.
It is a new era. We have more tools, obviously, for our patients. It means one more drug, and that’s always a challenge. We’ve already been doing the pillars of care. This is the fourth pillar of care, but now with a class 1A indication.
Take a look. They’re easy to read. Dr. McDonagh is the first author, and I think they’ve been extremely well done.
Dr. Piña is professor of medicine at Thomas Jefferson University Hospital in Philadelphia. She is a heart failure and cardiac transplantation expert. She disclosed serving as an adviser/consultant to the FDA’s Center for Devices and Radiological Health and has been a volunteer for the American Heart Association since 1982.
A version of this article appeared on Medscape.com.