#153 HFpEF: 5 Pearls Segment
Update: 2024-06-05
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Timestamps:
(01:59 ) | What causes HFpEF?
(11:22 ) | Does diastolic dysfunction imply HFpEF?
(19:21 ) | Is the BNP level helpful in HFpEF?
(25:06 ) | What scoring systems can be helpful in ruling in HFpEF?
(32:03 ) | What's the treatment for HFpEF?
Tags: cardiology, primary care, CoreIM, IMcore, nurse practitioner, physician assistant, hospital medicine, pharmacy, nursing education, heart failure with preserved ejection fraction
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Transcript
00:00:00
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00:00:55
This is a really confusing condition, so if you're confused, it's not because there's something wrong with your diagnostic abilities, it's that it's a very confusing condition.
00:01:04
That's Dr.
00:01:04
Emily Lau, a cardiologist at Mass General.
00:01:07
Welcome to the Coreium 5 Pearls Podcast, bringing you high-yield evidence-based pearls.
00:01:12
This is Dr.
00:01:13
Shreya Trubetti, and Dr.
00:01:14
Rati Vaughan, an internal medicine resident at Bethes Real Deaconess Medical Center.
00:01:19
And today, we will be focusing on heart failure with preserved ejection fraction, aka heath-path.
00:01:26
And hopefully, we will make this topic a little bit less confusing with what we do and what we don't know about heath-path.
00:01:32
So let's get started with the pearls that we'll be covering today.
00:01:35
Be sure to test yourself by pausing after each of the five questions, remember, the more you test yourself, the deeper your learning gains.
00:01:44
Pearl 1 - What is heath-path?
00:01:46
What causes heath-path and what are the biggest risk factors?
00:01:55
Pearl 2 - Echo findings and diastolic dysfunction.
00:02:00
Does diastolic dysfunction imply heath-path?
00:02:03
And what are the typical echo findings in patients with heath-path?
00:02:13
Pearl 3 - BNP What are BNP levels influenced by, and is a BNP level helpful in heath-path?
00:02:27
Pearl 4 - Advanced Testing What scoring systems can be helpful in ruling in heath-path?
00:02:34
And what are other imaging or testing that we can do when the diagnosis of heath-path is not as clear?
00:02:45
Pearl 5 - Treatments for Heath-path What's the first and second-line treatment for heath-path?
00:02:52
Alright, Rathi, you know, I was so surprised when we started this episode, a lot of my cardiology friends said, "Heath-path, you're doing that topic?"
00:03:02
That's probably one of the hardest topics to cover, and I was like, "Really, heath-path, the thing that's in everybody's one-liners?"
00:03:08
I know, so it turns out the heath-path is such a heterogeneous disease, and we actually just don't know a lot about it.
00:03:15
So, a lot of preparing for this episode has actually been unlearning what I had associated with heath-path before.
00:03:22
Pearl 4 - Needless to say, we were ready for this challenge to clarify the murkiness around heath-path, and we're so excited to share what we learned, and as Rathi just mentioned, a lot of what we unlearned,
00:03:33
so to start off, in the most simple terms, heath-path is the clinical syndrome of heart failure with an EF of 50% or higher.
00:03:43
Heart failure in and of itself is a syndrome, and in cardiology we have few syndromes, so in its broadest sense, heart failure with preserved ejection fraction is defined as a clinical syndrome,
00:03:55
most commonly which presents with dyspnea either at rest or with exertion, that is due to a rise typically in left ventricular filling pressures at rest or with exercise.
00:04:09
That's Dr.
00:04:10
Ravi Patel, a cardiologist and director of the heath-path program at Northwestern, and these definitions make heath-path seem so straightforward, right?
00:04:18
But now that we know more, I want to put a huge highlighter like med school level double underlying the word syndrome with heath-path syndrome.
00:04:27
I do think in general when we're talking about heath-path, we're not talking about conditions with known ideologies, we're really talking about this kind of umbrella term,
00:04:38
poorly understood systemic disorder condition, and this is why this is one of the hot topics in the cardiovascular community today, because we simply don't understand this condition at all.
00:04:49
We don't yet have a consensus on how to diagnose this condition, it's probably multiple conditions all under an umbrella term of heath-path and understanding and sort of respecting the ambiguity I think is actually an important principle.
00:05:03
And to clarify why this heath-path syndrome is poorly understood and a systemic disorder, we have to first understand how heath-path even develops.
00:05:13
Dr.
00:05:13
Jen Ho, an advanced heart failure and transplant cardiologist at BIDMC did a great job explaining so succinctly just that.
00:05:22
So the pathogenesis of heath-path is really complex.
00:05:27
I'm not sure anybody fully understands what happens.
00:05:31
We used to think of heath-path really as a disease related to hypertension and hypertensive LV remodeling that leads to LV stiffness.
00:05:42
And I think this has really shifted more recently to this idea that it happens in multi-morbid patients with central contributions from obesity and cardiovascular disease.
00:05:55
We think that those predisposing factors probably incite systemic inflammation that then leads to endocelial dysfunction and altered myocardial energetics and abnormalities and skeletal muscle.
00:06:09
And so it's a lot more complicated, I think, than we initially appreciated.
00:06:14
OK, so on to unlearning point number one.
00:06:17
Heath-path is not that classic high blood pressure causing stiff ventricles that we may have learned about back in the day.
00:06:23
Heath-path is so much more.
00:06:25
And what really stood out to me is that it's not the heart as the initial culprit in the classic garden variety heath-path.
00:06:32
Whereas in garden variety heath-path, you're talking about a culmination of one's cardiomyabolic risk profile that then seems to activate inflammation, that then leads to all these downstream sequelae,
00:06:43
that then lead to structural changes and functional changes in the heart that can then contribute to the syndrome of signs and symptoms of heart failure and preserve ejection fraction.
00:06:54
As we think of heath-path as a syndrome from the outside in that's affecting the heart, as opposed to heath-graph, which is an intrinsic myocardial process, then exhibits negative effects to all other organ systems.
00:07:07
I love that comparison of heath-path to heath-graph.
00:07:11
And also for those of you that are not in the know, heath-graph is what the cool kids say, as heart failure with reduced ejection fraction.
00:07:17
Thank you so much for clarifying Shia.
00:07:19
I hope it's mostly the cool kids listening to us.
00:07:22
But we can pretty much think of heath-graph as a central cardiac disorder, where after the EF takes a hit, there are all of these downstream effects on other organ systems.
00:07:33
But with heath-path, it starts as a systemic disorder, with all of these outside cardiometabolic risk factors, like obesity, pre-diabetes, hypertension,
00:07:43
and all of those kind of come together and lead to this pathogenesis that nobody fully understands, but has something to do with inflammation, and that then affects the heart.
00:07:54
Yeah, you don't know that.
00:07:55
I think about it.
00:07:55
All the classic one-liners for most of our patients is like 72-year-old woman with hypertension, hyperlipidemia, type 2 diabetes, and heath-path presence with X, Y, and Z.
00:08:05
So your one-liner there actually highlights another big risk factor, an older person.
00:08:11
Heath-path is outstripping heath-graph as the most common type of heart failure, and as we get older, our immune systems change, there is more adverse inflammation that may occur,
00:08:22
and there is an accrual of co-orbidities as well that can ultimately lead more likely to heath-path than heath-graph.
00:08:28
Wow, so interesting, I think that people, as they get older, their immune systems change, and how we may be prone to more inflammation with just natural aging, and that contributes to this syndrome.
00:08:38
I know, and there's actually also one other demographic risk factor that I wanted to bring up, because it was actually one of the reasons why I chose this topic.
00:08:47
Oh yeah, which one is that, Rathy?
00:08:49
So heath-path affects a higher proportion of women compared to men.
00:08:53
Dr.
00:08:54
Lau has a clinical interest in this, so I was really excited to pick her brain and see what she's thinking about this trend.
00:09:00
We're increasingly also beginning to recognize that there are other female specific risk factors like history at pre-clampsia, which may also be related to heath-path, and so it really underscores this idea that heath-path is really a systemic condition.
00:09:15
Oh man, I'm just trying to wrap my head around how certain aspects of pregnancy, like hypertensive disorders, like pre-clampsia, and those things might make someone different in terms of inflammation,
00:09:26
and what that means later with these increasing proportions of women developing heath-path.
00:09:31
Yeah, so if we think back, rewind your brain back to med school, think about the pathogenesis of pre-clampsia, we can remember it involves systemic inflammation and endothelial dysfunction.
00:09:43
So when you see it like that, it kind of makes sense that we have this connection with the path path, and the caveat we should say is there is still a lot left to be uncovered about these female specific risk factors.
00:09:54
Yeah, I guess caveat to side, it seems like inflammation just is all over and is rearing its head again.
00:10:00
I think, again, it really reiterates to me the biggest takeaway is to change my one-liners from just half-path to say, "Heath-path syndrome to really do it justice."
00:10:09
So to summarize what I've learned about, "Heath-path syndrome," see what you did there.
00:10:13
Thank you.
00:10:14
The systemic disorder that is the culmination of a patient's cardiometabolic risk factors and even things we don't fully understand related to pregnancy.
00:10:23
All of that activates inflammation and endothelial dysfunction, which then alters the structure of the heart.
00:10:29
And then the structural changes in the heart lead to a rise in LV pressure either at rest or with exercise.
00:10:35
And then before we close out this pearl on what "Heath-path" is, we should caveat that there's tons of "Heath-path" quote-unquote, "masqueraders."
00:10:42
And it's not all the classic garden variety, "Heath-path" that we've been talking about right, the typical patients who have hypertension obesity diabetes.
00:10:50
Yeah.
00:10:51
And "Heath-path" has such a broad definition, it's hard not to label everyone with it because almost everybody that comes into the hospital has a little bit of dysmia.
00:11:00
Most of them have an EF greater than 50 percent.
00:11:02
Now, something that comes up a lot in terms of diagnostic workup is that there are things that can look like "Heath-path" that we call "Heath-path" masqueraders that can cause heart failure with normal ejection fraction.
00:11:15
And so it's really important to try to identify and differentiate "Heath-path" masqueraders from what I call "garden variety" "Heath-path" because the management is often really different.
00:11:26
Serosis, nephrodics, syndrome are things that you know you'd be surprised, but sometimes come into my clinic and our build is potentially "Heath-path."
00:11:35
It's kind of crazy to actually think through the list of things that can cause a little dysmia.
00:11:40
I wouldn't even know where to begin.
00:11:41
Yeah, it is.
00:11:42
I think maybe one branch point is to separate out the cardiac "Heath-path" masqueraders versus the noncardiac "Heath-path" masqueraders.
00:11:49
And so typical cardiac masqueraders include things like amyloidosis, sarcoidosis, valvular disease.
00:11:55
The noncardiac masqueraders are the things that Dr.
00:11:57
Patel just mentioned right, nephrodics syndrome, cirrhosis, anemia, of course, anything with the lungs.
00:12:03
Our reviewers actually pointed out how we need more on "Heath-path" masqueraders, and we honestly just weren't able to cover it all in this episode, so just look out for a bonus episode on "Heath-path" masqueraders.
00:12:18
So since the syndrome is so heterogeneous, let's dig into the objective data that can make us more confident when we're trying to figure out does someone have "Heath-path" do they not have "Heath-path"? Yes.
00:12:29
Yes.
00:12:30
Let's get into all things echoes.
00:12:31
Finally.
00:12:32
I bet that makes your cardiology heart very happy, Robby.
00:12:37
It sure does.
00:12:38
So with the echo, we can first look at diastole, and diastole is the ability of the heart to relax to fill with blood.
00:12:45
And then the term that we always hear with "Heath-path" is diastolic dysfunction, but I think the money question is, does diastog dysfunction mean slam dunk "Heath-path"? I always go back to the classic physiologic definition of heart failure,
00:13:01
which is the inability of the heart to meet the metabolic demands of the body or to do so at the expense of elevated filling pressures.
00:13:08
And so it's a clinical syndrome at the heart of it.
00:13:11
So if you just have an imaging finding of diastolic dysfunction, but the person doesn't have any symptoms of heart failure, can exercise, you know, run five miles, that is not "Heath-path" by definition,
00:13:25
right?
00:13:26
Okay.
00:13:27
Unlearning point number two.
00:13:28
I think I'd like to repeat this to myself a bunch, "Heath-path" and diastolic dysfunction are not synonymous terms.
00:13:35
Diastolic dysfunction is an abnormality with relaxation or filling that is separate from "Heath-path" syndrome, which requires clinical symptoms.
00:13:44
Now invariably, diastolic dysfunction is an important component.
00:13:48
We know patients with heart failure with preserved ejection fraction have LV stiffness as a big problem that really makes them exercise intolerant.
00:13:58
And so this is a really complex issue.
00:14:00
I would look at them as slightly overlapping Venn diagrams.
00:14:05
There are people that have both, but having diastolic dysfunction does not mean you have "Heath-path" automatically in the absence of the clinical syndrome.
00:14:13
This brings up "Unlearning point" number three.
00:14:24
But that was not the right way to think about it.
00:14:27
So you can have "Heath-path" without diastolic dysfunction, and it is quite common.
00:14:32
We see it more and more.
00:14:34
Diastology and the assessment of diastology is one aspect of understanding that an individual has "Heath-path" but it's not the whole story.
00:14:42
What we've come to realize is that while diastolic dysfunction is prevalent in many patients with "Heath-path," there are also many patients who do not have that same delayed relaxation of the heart,
00:14:54
that true diastolic dysfunction as you would measure it on an echocardiogram, but still have a syndrome of heart failure, which is a rise in left ventricular filling pressures at rest or with exercise.
00:15:05
That's so interesting.
00:15:08
I actually started reading into that, and I was surprised to learn that up to one third of patients with "Heath-path" don't have diastolic dysfunction on their resting echocardiograms.
00:15:17
Yeah, and this may be getting too much into the weeds, but if you are someone who doesn't just like to look at the impressions, there's actually four specific things to look at on an echo to determine diastolic dysfunction.
00:15:27
We'll link more in the show notes, of course, but just like big picture, what are those four things?
00:15:32
One, LA enlargement, or the LA volume index, to the EVE prime being greater than 12 to 14, which just means how hard is that left side of the heart working to pump blood,
00:15:43
three looking at tissue doppler velocities, particularly the septal and lateral E prime velocity, and then lastly the TR velocity.
00:15:50
And if three or more of those are abnormal on the echo, that's diastolic dysfunction.
00:15:56
If two are abnormal, it's "indeterminate."
00:15:59
The other point to keep in mind with echo is it can be helpful when it's abnormal.
00:16:05
However, some people with hef-pef can actually have normal echoes as well.
00:16:11
So that's what makes it really, really tricky.
00:16:14
Wait, wait, wait, wait.
00:16:16
Okay.
00:16:17
So we just went over that patients with hef-pef do not necessarily have diastolic dysfunction, but now you're telling me that some patients with hef-pef have no abnormal finding on echo?
00:16:43
That's exactly what we mean, and this blew my mind too.
00:16:56
But again, echo is not a gold standard diagnostic test for hef-pef.
00:17:01
Some people for all intents and purposes can have normal looking echoes and still have the clinical syndrome of hef-pef.
00:17:07
So that's, I think, another challenge in this field.
00:17:10
Oh, yeah.
00:17:11
Another wrench to throw into the diagnostic challenge.
00:17:15
And I really like cardiology because I really like when things make sense.
00:17:19
So I just, I loved how Dr.
00:17:20
Patel explained how particularly patients with obesity might have normal echoes.
00:17:26
Essentially, there's a syndrome that we are beginning to see where, especially in obese patients, where patients' hearts are just essentially mismatched in terms of size.
00:17:37
So their LV size is just not big enough to handle the amount of circulating blood volume that they have.
00:17:43
As a result, they might not have elevations and filling pressures at rest, but when they exercise and more circulating blood volume is required, they will have elevations in their wedge pressure and symptoms of dyspnea.
00:17:55
So another way to frame this is that the heart can't supply the metabolic demands of the body in obesity.
00:18:01
And this can lead to a high output heart failure, which can actually be considered a subset of hef-pef.
00:18:07
Oh, yeah.
00:18:08
So I guess you're saying that, you know, in patients who have obesity, there's more cells, and that's creating more demand and that can lead to the classic symptoms of heart failure.
00:18:16
That's a great way to put it.
00:18:18
So often patients with obesity will have normal echoes at rest, but then it's really when they're like getting up and on exertion that their LV can't compensate for these higher circulating volumes,
00:18:29
and that leads to the higher pressures we see.
00:18:32
You know, I used to think that someone could not have heart failure unless they had a large atrium and stiff ventricles, meaning their E to E prime ratio was like greater than 12 to 14,
00:18:42
but yeah, I realized that was not the case.
00:18:45
I'm totally with you there, Shrey.
00:18:47
I'm used to being on heart failure rounds and looking at echoes and pointing out how dilated the atria are.
00:18:53
So let's take a minute to talk a little bit more about the left atrium.
00:18:57
We assume that diastolic dysfunction is also resulting in certain aspects we see on an echocardiogram like left atrial enlargement.
00:19:07
Left atrial enlargement in and of itself does not measure anything with regard to diastology, it's felt to be a surrogate for chronically elevated left ventricular failing pressures, and the same goes for pulmonary artery or right ventricular systolic pressures on echo,
00:19:21
which we use as a surrogate for diastolic dysfunction.
00:19:25
It looks like all of these echo findings tie together, and none of them in particular give us a clear picture on their own.
00:19:31
So patients would have, if they can have a clear combination of all of these findings, but they could also have none of these findings at all.
00:19:39
Yeah, it is a hard topic, but let's try to summarize what we're taking away.
00:19:45
So we learned that having diastolic dysfunction doesn't label someone as heft path, and on the flip side, we also learned that not having diastolic dysfunction on the echo doesn't not mean heft path.
00:19:57
A patient needs to have the clinical syndrome of volume overload and elevated left to filling pressures at rest or with exercise, which we talked about in obesity, and they can have completely normal echoes,
00:20:08
meaning normal L.A.
00:20:10
sizes and all those e-prime velocities.
00:20:16
So that was all echoes.
00:20:18
What about brain-naturetic peptides?
00:20:20
BNPs?
00:20:21
Can that help us out with something a bit more objective when it comes to heft path?
00:20:26
BNP is a very unique hormone.
00:20:29
It's obviously one that's created by the heart, and its secretion is stimulated by wall stress.
00:20:37
So wall stress of the LV, wall stress of the L.A.
00:20:39
and potentially R.V.
00:20:41
will contribute to elevation in BNP, so if one is potentially congested, BNP will go up as a result of wall stress.
00:20:52
So that all makes sense in theory.
00:20:54
The wall stress means that the BNP should be elevated, and technically, this should be able to help us out with the diagnosis of heft path.
00:21:03
There are various different reasons why you can have an elevated, natuotic peptide level.
00:21:07
The most typical reason is with cardiac stretch, and so that's what makes it such a good marker of heart failure.
00:21:14
So we know that, of course, in patients presenting with dysnia and suspected heart failure, natuotic peptides are sort of the central test that we send to try to verify whether or not they have heart failure.
00:21:27
I think certainly in the setting of chronic kidney disease and the setting of atrial fibrillation, your natuotic peptide levels can often be more elevated than what we would typically see.
00:21:37
In just volume overload states, women typically have higher natuotic peptide levels compared with men in general, so I think that's so fascinating, we don't really know why.
00:21:48
And then I guess the flip side, similar to echo, a normal natuotic peptide level, unfortunately, is not awesome at rolling out heft path.
00:22:01
Bummer.
00:22:02
It sounds like B&P by itself is another test that can be helpful, but it's just one more piece of the puzzle.
00:22:09
Bradley, can you help us kind of make it all make sense a little bit?
00:22:13
Why would a B&P be normal in some patients with a heft path?
00:22:17
So what I learned from talking to our experts is that anti-proBNP is influenced by all sorts of factors like age, obesity, or as Dr.
00:22:25
Home mentioned, atrial fibrillation and kidney disease.
00:22:29
So it sounds like most of these confounders are related to the garden variety, patient who has heft path, especially being with the metabolic syndrome and all, so I can see how things kind of add up to be a bit tricky.
00:22:39
Yeah, and I guess even trickier, because one surprise in confounder I learned is our patients with hypertension over time, they develop LV hypertrophy, and that actually ends up lowering the B&P.
00:22:51
Hypertrophy of the LV will actually create less wall stress.
00:22:55
So a condition that is very common in heft path can actually paradoxically result in lower B&P.
00:23:04
So the stimulus for B&P going up, which has increased wall stress, goes down in the setting of LVH.
00:23:09
So that's one reason why it's not as helpful or it might not rise as much.
00:23:15
The second is the clearance of B&P, which we think is due to adipose tissue.
00:23:19
We think adipose tissue clears natural peptides out of the circulation.
00:23:23
So in patients who are obese, they may have lower B&P because that B&P is being cleared more quickly.
00:23:30
Oh, this is such interesting physiology when there's left ventricular hypertrophy that decreases wall stress and then less B&P might get leaked out and adipose tissue on top of that clears the B&P.
00:23:42
And then I also learned a new term that was pretty interesting, B&P deficiency.
00:23:48
There's thought that potentially there are patients who are B&P deficient.
00:23:52
B&P is a marker, but as a hormone in its function, it's a B-type naturaletic peptide.
00:23:59
It results in naturalesis.
00:24:00
It's a vasodilatory hormone that is a beneficial hormone.
00:24:05
We've studied naturaletic peptide analogs as therapies for heart failure.
00:24:10
And so there's a thought that there are some patients who don't secrete enough B&P and their B&P is low, and that might actually drive some of their heart failure that they don't have this beneficial hormone.
00:24:21
And so that's why we don't see it in the circulation.
00:24:23
That's such a new way of thinking about B&P as a helpful hormone in heart failure.
00:24:29
I'm just so used to seeing an elevated B&P and thinking, "Oh, no, but maybe I should actually be more concerned when I'm looking at a patient and they're clearly volume overloaded to me."
00:24:40
But then I turn and look at the computer and I see that the B&P is really surprisingly low.
00:24:46
We know there are patients who have a naturaletic peptide deficiency, we call it.
00:24:51
They can often have very low naturaletic peptide levels despite being very volume overloaded.
00:24:58
In some studies, we think this is tied to having obesity.
00:25:03
Some of it might be related to insulin resistance as well.
00:25:07
And we know there are naturaletic peptide gene variants that can often affect your natural levels of naturaletic peptides and cause some variation between individuals, even now these states.
00:25:18
So all of those reasons are potential ideologies for naturaletic peptide deficiency and so when you see a normal B&P in someone presenting with true clinical heart failure,
00:25:30
they still have true clinical heart failure.
00:25:32
Okay.
00:25:33
Cedar recap.
00:25:34
B&Ps are normally produced and released when there's increased myocardial wall stress.
00:25:40
But the B&P level can be normal in half path, especially when there is left ventricular hypertrophy that's been going on for a while or obesity.
00:25:49
The last interesting thought to end with is that there's actually B&P deficiency, which can actually leave some of our patients more susceptible to volume and pressure overload.
00:26:02
Before we get into advanced testing for half path, it might be helpful to recap the big picture of where we are.
00:26:08
I think that PEPP is a very unique syndrome in cardiology.
00:26:14
Again, we don't have one diagnostic test.
00:26:16
I am very, very reticent to rule out the diagnosis of PEPP based off of a single test, whether it be a B&P and echocardiogram,
00:26:27
specifically those two criteria.
00:26:30
And I would say that that's one of the things that I've learned a lot is that there's no one test to rule in, but there should be no one test to rule out, either.
00:26:40
So if there is a patient that you see in clinic that is complaining of shortness of breath, and things don't smell cardiac based off of laboratory testing or echocardiographic testing,
00:26:52
just be mindful that there is a possibility that it is still PEPP that's lurking.
00:26:59
So there's a lot of clinical gestalt and factors you're weighing together when you're thinking about PEPP.
00:27:05
And it just makes me wonder, are there any helpful PEPP risk calculators that can guide us one way or the other?
00:27:11
I do think the risk scores may be helpful when the diagnosis isn't clear based on your first-tier testing.
00:27:17
So your first-tier testing, I would say, is your clinical exam, your history, naturopeptides and PEPO.
00:27:24
If after that the diagnosis is still not clear, I think potentially getting some sense from these diagnostic scores of risk stratification can be helpful.
00:27:34
We asked Dr.
00:27:35
Ho to tell us a little bit more about these risk calculators and how to use them, one to use them, if we should even be using them.
00:27:43
There are two diagnostic scoring algorithms that have been developed in recent years.
00:27:50
One is called the H2F PEPF score, and the second is called the HFA PEPF score.
00:27:55
And the idea of both of these scores is that they incorporate colorbid conditions plus naturopeptides plus echo findings to kind of risk stratified people.
00:28:08
And if you have a low risk score, you effectively rule out HFA PEPF.
00:28:14
If you have a high risk score, you effectively rule it in.
00:28:17
And if you're intermediate, those are the people where we may want to consider pursuing advanced testing.
00:28:23
So those are the two scores.
00:28:25
I would say that there's some potential for misclassification with these scores.
00:28:32
And so we just have to be cautious.
00:28:34
For example, the H2F PEPF score was developed in the Mayo Clinic where people get referred if there's a question for HFA.
00:28:44
And so the pre-test probability walking in the door of somebody having HFAF was something like 60% or greater.
00:28:51
Okay.
00:28:52
So we have to think carefully about who we invoke these risk calculators on.
00:28:56
So I'm curious then, who is it useful for?
00:29:00
But there are people who do walk around with HFAF PEPF, who may not be hospitalized frequently if at all.
00:29:07
And this score can be extremely useful for them.
00:29:09
So I use it in the outpatient setting, a lot among patients who have never been hospitalized and are having dyspnea-related syndromes and have seen pulmonary or seeing me and have not had a diagnosis made.
00:29:23
I'll use this as a screening tool to say, well, what's the probability of having HFAF?
00:29:27
So in some cases, when it's really hard to tease out, is this HFAF, is it not?
00:29:32
And especially if the patient's exam is tough to tell if their volume overloaded and their symptoms are kind of vague, then it's helpful to reach for some more advanced testing options like right heart cath or cardiac MRIs.
00:29:44
There are cases that are challenging where the diagnosis is still not clear.
00:29:49
You're not really sure where the JVP is, it's hard to see.
00:29:52
And in that setting, if the diagnosis is still not clear, I do think I sometimes turn to what I call advanced testing, and that can involve invasive hemodynamic testing.
00:30:04
So we can do, for example, a right heart catheterization to assure that what we think is the JVP on exam is actually evidence of elevated filling pressures in somebody.
00:30:13
And so that might be really helpful to confirm your diagnosis in cases when you're still not sure.
00:30:21
And the exam maybe is not so clear.
00:30:23
Man, can I just say how validated I feel when cardiology sees one of my patients?
00:30:30
And they're also like, "Hmm, yeah, that exam's hard."
00:30:33
Recommend right heart catheter.
00:30:34
I'm like, "Yes, please.
00:30:35
Thank you."
00:30:36
I know exactly how you feel, and especially when you have a patient who only has symptoms with exertion.
00:30:44
So patients often feel fine at rest, but with exercise, they get short of breath.
00:30:49
And it's often not diagnostic when all of our diagnostic tests are when the patient is lying down in the left lateral to cubitous position, that we're going to be able to identify the syndrome.
00:31:00
It's a syndrome that is exertional, it's a syndrome that is exercised induced.
00:31:05
And so a lot of times we have to bring a patient to the cath lab, put a right heart catheter procedure and get that done, understand what their physiology is when we perturb the system,
00:31:16
when we exercise them, to really understand what's going on.
00:31:20
And that's not easy to tell in clinic.
00:31:23
Wow, I have never heard of someone exercising during a right heart catheter.
00:31:28
Dr.
00:31:28
Ho did agree that it's a pretty good provocative maneuver, but she did also share some other options in case exercising is impossible.
00:31:37
The other provocative maneuvers that have been studied in that setting are either passive leg rates.
00:31:43
So it turns out that even with passive leg rates and increasing your venous return, sometimes you can sort of provoke an abnormal response.
00:31:50
And then the other potential maneuver to consider is volume challenge.
00:31:55
So you can give them some ibifluid and sort of see, do they have, again, it's like a very exorbitant rise in lb-fluent pressures that indicates lb stiffness.
00:32:02
Okay, so that's the right heart cath.
00:32:05
What about cardiac MRIs?
00:32:07
When can that be helpful?
00:32:09
So cardiac MRI or other advanced testing isn't required for diagnosis of HEPF, but cardiac MRI can be really helpful to investigate those HEPF mask radars we talked about way at the beginning,
00:32:21
like amyloidosis.
00:32:22
Okay, so it sounds like cardiac MRIs aren't necessarily going to give us more information about the typical garden variety HEPF that we've been talking about for most this episode.
00:32:32
It's really going to be more helpful in investigating HEPF mask radars, which definitely kind of changes management of things.
00:32:37
So to wrap up this crawl, we talked about risk calculators for HEPF, which is typically used in more ambiguous cases in the outpatient setting where you're suspicious of possible HEPF.
00:32:47
And then for particularly tricky cases, we can reach for other things like right heart cats, especially when we want to provoke symptoms during exercise.
00:32:58
Okay, now that we have unlearned a ton when it comes to the diagnosis of HEPF, I've lost count of how much I have unlearned, let's round things out with a bit more on management of HEPF.
00:33:11
HEPF is a disease of multi morbidity.
00:33:15
And so often it's really hard to completely attribute someone's symptoms to one single cause alone, right?
00:33:24
And we see patients who have obesity, plus HEPF, plus COPD, plus diabetes and hypertension and maybe some valvular component to this as well.
00:33:40
And I think it's really challenging and often impossible to kind of pinpoint your finger as to one ideology that's going to fix all of their symptoms because often they're presenting with multi morbid conditions.
00:33:56
And so really making sure we're treating their hypertension, their coronary disease, we've optimized their diabetes treatment, we're thinking about obesity, so all of those things are really important.
00:34:06
I really appreciate how Dr.
00:34:08
Ho talks about treating risk factors as part of the management so explicitly.
00:34:13
I know that when I look at notes and under the hashtag #HEPFProblem, I rarely see focusing on risk factors for HEPF.
00:34:20
Yeah, that's same.
00:34:21
I'm glad we went over that, so think else that I think I can change in addition to HEPF syndrome, kind of making sure there's a risk factor point in there.
00:34:30
With that being said, let's move on to medications for the true clinical HEPF.
00:34:35
I know when it comes to heart failure with reduced suggestion for action, those seem a bit more straightforward with a GDMT that we have, but I'm curious kind of with HEPF, what's the treatment that we actually have on deck here?
00:34:47
In terms of a general approach, I would say I typically consider SGLC2 inhibitors broadly in everyone with HEPF.
00:34:56
When there's congestion present, I actually really like potentially considering upfront mineralic record receptor antagonists because they can treat some of the congestion and may minimize your use of the loop diuretic,
00:35:09
but if people still have congestion, then of course we're using loop diuretics.
00:35:13
And then in the setting of persistent symptoms with blood pressure room, I would consider RNA.
00:35:18
Okay.
00:35:19
So the key players in HEPF are SGLC2 inhibitors and mineralic record-acquired receptor antagonists, aka MRAs.
00:35:26
We can also think about RNAs, especially if blood pressures in a shoe, and then we cannot leave out the huge utility that we get from loop diuretics for symptom management.
00:35:36
With all that kind of laid out, let's take a closer look then to the first line treatment in HEPF SGLC2 inhibitors.
00:35:43
There have been two pivotal trials that have really put SGLC2 inhibitors on the map as first line for anybody with HEPF.
00:35:52
Those two trials were emperor preserved and delivered, and they looked at treatment with either empagloflosin or dipagloflosin.
00:36:00
So these studies show that empagloflosin decrease the risk of heart failure hospitalization and cardiovascular mortality.
00:36:06
We love that.
00:36:07
And this is, again, in patients with HEPF as well as heart failure with mid-range ejection fraction, which has a cutoff of EF greater than 40 percent.
00:36:16
I think the cool kids say HEPF MRAF for that?
00:36:19
Amarathi, is that correct?
00:36:21
Yeah, as a cool kid myself, I would say HEPF MRAF.
00:36:25
Nice.
00:36:26
You're definitely more than know than most of us, thanks, Cheyah, and to build off of that.
00:36:32
The second line treatments after an SGLC2 inhibitors added include both an MRA and an RNA.
00:36:38
Yeah.
00:36:39
In the MRA, we know from the top cat trial that Sprone Electron is associated with a small reduction in cardiovascular hospitalizations.
00:36:46
Yeah, but Sprone Electron didn't reduce cardiovascular deaths and HEPF in that trial.
00:36:51
Okay.
00:36:52
That's all good to know.
00:36:53
And then what about RNAs?
00:36:54
What are we reaching for that and what's the story behind why RNAs kind of made it into the second line?
00:37:01
Angeotinson receptor number lysine inhibitors are RNA.
00:37:04
The trial that looked at the use of these agents is called Paragon HF.
00:37:08
The overall trial was neutral, but subgroup analyses showed some potential benefit in people with what they called the low normal EF, and interestingly also benefit among women compared with men.
00:37:20
So currently, RNA use deserves a class to be indication in the U.S.
00:37:25
guidelines.
00:37:26
And I would say that we're using them mostly in people who have persistent symptoms on an SGLC2 inhibitor, who also have evidence of hypertension.
00:37:36
And in particular, in people with the low normal EF or in this awkward category of heart failure with mid-range EF.
00:37:44
Okay.
00:37:45
So RNAs for heart failure, so Kubutova Valsartin or Intresto, didn't reduce heart failure admissions or cardiovascular mortality more than Valsartin alone.
00:37:56
But the good thing was that the RNA group did have improvements in symptoms.
00:38:01
I do have to take a moment to point out here, Shia, that it's really fascinating what Dr.
00:38:06
Ho mentioned, that Paragon HF showed how RNAs led to a reduction in heart failure hospitalizations and cardiovascular mortality in women, but it didn't do the same thing for men.
00:38:18
Yeah.
00:38:19
That is really interesting to say.
00:38:20
And again, it's all subgroup analyses, but maybe this is a good point to recap treatment of HF PATH.
00:38:25
First and foremost, it goes without saying that we need to address risk factors of HF PATH.
00:38:30
We just don't want to throw on medications, right?
00:38:33
But then when it comes to meds, our first sign treatment in HF PATH is going to be the estueltitude inhibitor, and then after that, we can either add a mineralocorticoid receptor antagonist if there's congestion or an RNA if the patient has a slightly lower EF or maybe in women,
00:38:49
though, again, this is all kind of subgroup analysis, and the data is just more for us to consider than like a hard recommendation.
00:38:56
As we keep learning more about HF PATH, there's going to be even more to consider.
00:39:00
So, you know how we hear about GLP1 agonist all the time now.
00:39:04
Oh, all the time, yeah, definitely.
00:39:07
So it's not really surprising that they have a role here as well.
00:39:11
There's a lot of excitement around an evolving role of GLP1 receptor agonists.
00:39:19
There were some promising data recently published and presented with a trial called "Step HF PATH" that showed that GLP1 receptor agonists in patients with HF PATH resulted in a sustained weight loss,
00:39:32
but also really remarkable improvements in quality of life and also six-minute walk distance.
00:39:39
We don't have trials powered on outcomes just yet, but I think this will be a quickly evolving landscape.
00:39:47
And like all things in cardiology, there's just so much research, and I'm sure the landscape will evolve rapidly and will have data on GLP1s when it comes to hospitalizations and mortality and all the things we care about pretty soon.
00:40:01
And on that note, that's a wrap for today's episode.
00:40:03
Please share this with your colleagues or anyone else who you think may find this episode helpful.
00:40:07
Please check out our YouTube channel for some behind-the-scenes interview content that didn't make it on air, but was still so good.
00:40:13
And a huge thank you to our reviewers, Dr.
00:40:15
Greg Katz, Dr.
00:40:16
Snaehlbot, and Dr.
00:40:18
Randy Goldberg.
00:40:19
This episode was made in part from the Digital Education Track at BIDNC.
00:40:24
Thank you so much to all the mentors involved in this work.
00:40:27
And thank you, Dr.
00:40:28
Patia, for the audio editing as well as to Dr.
00:40:30
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00:40:32
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00:40:37
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