This transcript was automatically generated from the video recording and may contain inaccuracies, including errors or typographical mistakes.

Dr. Pam Taub (UC San Diego Health System): Let us get started by talking about early signals to make sure that we diagnose heart failure early and we intervene early. The focus in our field has really shifted from what I call secondary prevention or treating disease once it is manifest. That goes for patients with atherosclerotic cardiovascular disease and also for heart failure.

Why should we wait for the first heart failure admission or repeated heart failure admissions to really diagnose and manage these patients. We need to be really moving upstream and diagnosing early when their subclinical features and preventing that first heart failure admission.

Interdependent Pathophysiology of DM, CKD, and HF

One of the things that has been really incredible over the past decade is our appreciation of how interconnected the organs are. If you think about the way we used to practice 15 years ago, everybody was in their silos. The cardiology clinicians would just be thinking about the heart and saying anything related to diabetes, that is not my organ.

The nephrologist would be thinking about the kidney and would not be thinking about the heart. We were not really communicating well.

A lot of the data that has emerged over the past 15 years has really changed that paradigm. What we realize is there is so much organ crosstalk and the organs do not operate in silos. They are constantly interacting with each other. There is a lot of feedback. Similarly, that is the way we should operate clinically. We should be talking to different specialties. We should be taking a multidisciplinary approach, and we should be getting feedback from each other and improving our care and providing a holistic view of clinical medicine and holistic care for these patients.

When you look at underlying pathophysiology, whether it is the heart, the kidney, the pancreas, their shared underlying pathophysiological mechanisms, and that includes things such as increased inflammation. That is a systemic process and that affects all the organs when you have increased inflammation.

What is one of the reasons why people have increased inflammation? Obesity. Obesity is a big driver of inflammation. A significant portion of our population, over a third, has obesity. We also have other common pathophysiological drivers, like impaired endothelial dysfunction that drives hypertension. We also have dyslipidemia that drives atherosclerotic cardiovascular disease.

All of these organs are really living in this milieu of shared pathophysiologic abnormal mechanisms that are driving disease. We need to be really cognizant about these underlying mechanisms and we need to address these mechanisms early.

Connecting Early Signals to Timely Intervention in HF

One of the key shifts that is occurring is how do we diagnose disease early? We are also recognizing that, especially in our management of heart failure, that sometimes the symptoms can be very subtle and it can be very non-specific, such as just fatigue, decreased exercise intolerance. A lot of times those symptoms are attributed to just aging, deconditioning, obesity. They can be heralding future heart failure events.

We also need to understand what the comorbidities are that predispose patients to heart failure. That includes diabetes, obesity, chronic kidney disease.

When we talk about chronic kidney disease, we should not be waiting for it to stare us in the face with an elevated creatinine or a decreased eGFR. We should be utilizing evidence-based tests, such as UACR to look for early signs of kidney disease. We need to do that test much more often in our patient population.

Too many patients are identified very late in the course of their disease and most heart failure patients are diagnosed with heart failure after they present to the emergency room with their first heart failure exacerbation. When you look back, you see that there is a lot of clues that were missed, including in patients who have had echocardiograms, where the ejection fraction is normal but subtle signs such as left atrial enlargement, left ventricular hypertrophy, changes in diastology just were under-recognized.

We have to do better. This whole new paradigm of looking at CKM as one unified disease entity is going to help us with this early identification of our patients.

A Systemic Disease Across a Continuum

As I said earlier, we have to think about CKM as a systemic disease that is impacting multiple organ systems. There might be something that manifests a little bit earlier. Maybe the first sign of CKM is insulin resistance or diabetes, but that should clue us in. This one organ is impacted, so the other organs are also living in this CKM milieu with shared underlying pathophysiological drivers of disease. We have to start thinking about these other organs.

When we think about heart failure, the easiest heart failure to recognize is heart failure with reduced ejection fraction, because we can see it on the echocardiogram. It is staring right at us. Then there is also heart failure with mildly reduced ejection fraction, about 41% to 49%. Sometimes we do not recognize this as a very serious condition. Sometimes we will say, “Oh, maybe the ejection fraction calculation is off and they do not need a defibrillator. They are pretty stable.” Sometimes we are not as aggressive with this mildly reduced ejection fraction, as we are with those patients with an ejection fraction less than 40%.

Then there is HFpEF, heart failure with preserved ejection fraction, which is completely underrecognized on echocardiogram because the report says normal ejection fraction. This is growing in prevalence and more women are impacted with HFpEF than with HFrEF. The outcomes for HFpEF are slightly worse than HFrEF. A lot of it has to do with the delayed diagnosis.

In terms of the underlying pathophysiological drivers of patients with HFpEF, if it is obesity, it is diabetes, it is CKD. Sometimes the HFpEF may not be evident, but all these other underlying comorbidities are there. We need to be thinking about HFpEF in our differential diagnosis of patients with symptoms that may be very non-specific and vague, such as just fatigue, decreased exercise tolerance, and we need to diagnose HFpEF earlier in the disease process.

Early Clinical Cues in HF

The clinical features are sometimes very subtle and that includes fatigue, orthopnea, mild edema. Sometimes we say, “Oh, you are just eating too much salt. You just need to reduce your salt intake.”

Sometimes it is very subtle symptoms. Like a year ago, I was walking a mile and a half, and now I am only able to walk a mile. Sometimes that is attributed to just, “Oh, you have gained weight, you are aging.” Sometimes people are just getting more bronchitis or they are getting more congestion and that could be a sign of pulmonary edema.

The thing that I see that is very confusing is a lot of people who have wheezing are diagnosed with asthma much later in life, and whenever someone is diagnosed with asthma later in life, you need to be thinking this is HFpEF. This is pulmonary edema that is manifesting as wheezing, cardiac asthma, as we call it.

We have to be really thinking more carefully about these subtle cues that these patients with heart failure, especially heart failure with preserved ejection fraction have.

Biomarkers and Imaging: Improving HF Diagnosis

There are tools that we can use. One of the best tools that we can use is a simple blood test, NT-proBNP or BNP natriuretic peptides. What they reflect is hemodynamic stress on the heart.

When you see even a mild elevation in these natriuretic peptides, it should clue you in that there is something abnormal. Patients with HFpEF do not have as dramatic elevations in their NT-proBNP as patients with HFrEF. This is why when you see even mild elevation, you should be thinking about HFpEF.

Then there are some caveats to natriuretic peptide interpretation. For instance, when someone is obese, the natriuretic peptide levels tend to be lower. So remember that. When someone has CKD or their age is increased, it can be a little bit higher. Just remember those caveats.

Even with those caveats, even mild elevations in natriuretic peptides should put HFpEF on your differential.

An echo is also very useful. The problem with echo is you have to look at some of the subtle clues on echocardiography, and sometimes it does not go into the conclusion part of the report, and that includes looking for left atrial enlargement. Even mild left atrial enlargement is a sign of diastolic dysfunction and HFpEF.

Looking for left ventricular hypertrophy that is very prevalent in patients with hypertension. When you see that, that should also clue you in. Then diastolic dysfunction. A lot of patients will have mild to moderate diastolic dysfunction on echo and they may be completely asymptomatic.

The real challenge is putting it all together because it is not one thing that is going to nail the diagnosis. It is really putting together what the symptoms are, what the exam is, the biomarkers. I would also look at kidney biomarkers such as EGFR, UACR to clue you in that this patient has CKD. Looking at markers of insulin resistance.

Sometimes these patients might have a normal hemoglobin A1C, but their fasting glucose is very elevated. Looking at all of those clues and then using imaging as well to put it all together to make the diagnosis.

Advanced Imaging and Risk Stratification Tools

There is other features on echo that we can use including global longitudinal strain. That is sometimes the first clue that there is a problem with heart function and sometimes that is also buried in the report. So you have to actually look for global longitudinal strain in the report.

Then there is also some great structured tools that we can use to help us diagnose HFpEF or if this patient is likely to have HFpEF. Those are some scores. One is the HFA-PEFF score, and the other one is the H2FPEF score. In these scores, you enter parameters like age, certain echocardiographic features, BMI, creatinine and then it will give you an analysis based on those features, whether this patient is likely to have HFpEF.

These tools are very useful, and some institutions have it integrated into the EMR to help with the HFpEF diagnosis.

The other group of patients that are very likely to have HFpEF is patients with atrial fibrillation. When you see someone with atrial fibrillation, chronic kidney disease, diabetes, think about HFpEF on the differential.

2026 CKM Risk Stratification: Identifying HF Earlier

We just got the new CKM guidelines that was just released about a month ago. This is really a big step forward for our field because it is really giving us a great framework by which to address these patients.

One of the key features of this guideline is the staging of CKM. Stage I is really looking at patients that have risk factors like obesity. As I mentioned earlier, obesity is a big driver of inflammation, and inflammation is a common pathway to atherosclerotic cardiovascular disease, heart failure, diabetes.

Stage I is where we need to really do a lot of lifestyle modification. Some of these patients might need pharmacotherapy.

When we get to stage II, these patients already have high blood pressure. They have signs of insulin resistance. This is where we want to intervene with certain strategic pharmacotherapy like SGLT2 inhibitors that can help with CKM, and also can help with so many other aspects of the stage II patient, including improving glycemic control.

Of course, GLP-1 receptor agonists that can help with weight management, but also can help with preventing progression of renal disease.

Both SGLT2 inhibitors and GLP-1 receptor agonists have great cardiovascular outcome trials showing that these drugs prevent or decrease cardiovascular events. The really new framing of the guidelines is in stage III, which is looking at patients that have subclinical disease, so they have not yet presented with their first myocardial infarction. They have not yet had their first heart failure admission, but they have all the features and they are at the tipping point of manifesting.

They are about to erupt. They are like a dormant volcano about to erupt. This is where you can use scores like the PREVENT score to help you stage these patients and to really estimate risk. Stage II and stage III are really the critical stages for us to intervene to prevent further manifestation of disease.

By the time there is stage IV, it is pretty obvious. I always say the art and elegance of clinical medicine is really in stages I to III, where it is not so obvious that these patients have disease. Of course, you want to continue longitudinal reassessment because people are evolving.

Another key feature of the guidelines that I really like is it talks about disease regression. If you intervene at the appropriate time. For instance, if you are intervening at stage II with maybe lifestyle therapy and SGLT2 and/or GLP-1 receptor agonists, people's disease can actually regress. People, for instance, with a GLP-1 receptor agonist, they will lose a substantial amount of weight. Their blood pressure is going to get better, their atherogenic lipids are going to get better.

The focus is not just on preventing progression. The new focus is regression of disease, and that requires early intervention.

Why Earlier Recognition Matters

The disease where early intervention is really paramount is heart failure. If we can recognize some of the comorbidities that these patients have and move heart failure, especially heart failure with preserved ejection fraction to the forefront of our differential diagnosis, we can diagnose these conditions much earlier.

Diagnosis and Treatment Delays Change HF Trajectory

When we diagnose disease earlier, we really prevent that awful disease trajectory that happens when people get hospitalized and they get repeat hospitalizations. Repeat hospitalizations are the worst. Every time someone gets re-hospitalized, their prognosis just gets worse and so many other things start to worsen, including their kidney function.

Early recognition, preventing that first heart failure hospitalization is so important.

GDMT Underuse: The Evidence–Practice Gap

Utilization of GDMT is also very important. If you look at so many of the current studies, even though we have these pillars of GDMT, especially for HFrEF, they are so underutilized. A lot of it is because of clinical inertia, and some of it is patient side effects and patients are not counselled appropriately. Some of it is access to care.

People are not being seen enough after hospitalization. This is where our APP community is so important, because so many of our discharge clinics are set up that are APP run, and this is where you are going to be seeing them first after their discharge. This is where we can intervene in making sure that they are adherent to the current GDMT that was initiated in the hospital. This is where we can add additional GDMT. This is where we build trust with the patient. This is where we have those conversations about if you are having a side effect, do not just stop the medication, let us know. Let us know what the side effect is and maybe we can adjust medications.

It is very critical that these discharge clinics are utilized across both community settings and academic settings. It is an important opportunity to prevent that next heart failure rehospitalization.

Key Therapies With Benefits Across the CKM Axis

We have already talked about SGLT2 inhibitors and incretin-based therapies. Incretin-based therapies are exploding. At the recent American Diabetes Association meeting, we had more data with a couple other agents that are incretin-based. One of them had weight loss in the mid 25% range.

In the next five years, we are going to see so many new therapies emerging in the incretin class. We already have many different SGLT2 inhibitors that have incredible data. The biggest issue is now implementation. When you think about any patient with heart failure, whether it is heart failure with preserved ejection fraction or reduced ejection fraction by guidelines, they need to be on an SGLT2 inhibitor.

We really need to make sure that this category of drugs is implemented across the heart failure spectrum. We know MRAs are very useful drugs, but we struggle with MRAs because of the hyperkalemia issue. We now have a nonsteroidal MRA that has great data and a little bit less incidence of hyperkalemia, but are very useful for patients with mildly reduced EF and also patients with HFpEF.

What is really revolutionary is if you think about 10 years ago, we had no FDA-approved therapies for HFpEF, and now we have SGLT2 inhibitors. We also have good data with the nonsteroidal MRAs. We now have evidence-based strategies for HFpEF.

SGLT2 Inhibitors Are Recommended in CKM Syndrome

SGLT2 inhibitors across the spectrum of ejection fraction, they should be used. They should be used in patients with CKD. Of course, for patients with diabetes that was the initial indication by which they were approved and also now in the hypertension guidelines.

Guideline-Concordant Therapy Pathways

We have gone through a lot and I hope there will be some questions about this. To summarize, we are in a new era, a revolution in cardiometabolic care, especially with our CKM guidelines. We should be using evidence-based therapies like SGLT2 inhibitors, GLP-1 receptor agonists, MRAs, including the nonsteroidal MRAs. Of course, utilizing RAAS inhibitors for CKD hypertension.

When we think about ASCVD utilizing statins. We also have so many non-statin options including ezetimibe and PCSK9 inhibitors.

Remember to use the PREVENT equation, that is now both in our CKM guidelines and in our lipid guidelines that were also released earlier this year. A lot of great therapies. The key is utilizing them and then getting our patients to comply.

From Early Signals to Earlier Action: Closing Gaps in CKM-HF Care  

I have given you a whirlwind about CKD, CKM, incretin therapy, SGLT2 inhibitors. Now, I am going to give it over to Stephanie to talk about action.

Dr. Stephanie Barnes (Duke University Health System): Thanks, Dr. Taub. For those who just joined us, please ask any questions that you may have in the iPads. Welcome to those who joined. We have an online audience as well.

I will run through these next slides about action. A case action for RNs and APPs to close gaps in CKM care, and we will move quickly because we have some fun cases that we will review.

Turning Early Signals Into Earlier Action

How do we turn early signals into earlier action? You heard about those subtle symptoms that patients with CKM develop early in their disease state. Recognizing that symptom drift and that patient-level reported decline is crucially important.

As you build relationships with patients and you know what matters to them, the activities that they do, documenting those throughout the continuum and flagging those profiles with heightened heart failure risk is increasingly important. That gradual decline in CKM conditions are really part of that signal. We hope that that is a key takeaway that you will bring today.

By identifying patients earlier for symptomatic decline, you are really helping that safe effective intervention across the continuum.

CKM Syndrome: Burden and Care Fragmentation

Now there is significant burdens in care fragmentation, and we know this right. Majority of this room are in the community. Some are in academic medical centers. From a statistics perspective, we know that about 40% of patients with type 2 diabetes and about 50% of patients with cardiovascular disease have comorbid CKD. So this disease state is not benign. It is pretty significant.

Care is fragmented. Even though you heard in an ideal world we would all be working together and in silos, care still remains fragmented and it can lead to delayed treatment. Those guidelines that you heard earlier, if you have not had the opportunity to take a look at those, please do so and really review the emphasis on that early screening, staging for your patients and coordinating care across disciplines, cardiology, nephrology, endocrinology and primary care to reduce those delays.

Just a pro tip is acknowledging that in a lot of our electronic medical records and our clinical notes, we identify who the primary care provider is. Do we do a good job if patients are seeing multiple disciplines of ensuring that the interdisciplinary disciplines are also documented in our clinical notes so that they can get the records from our care that day.

Interprofessional Workflow Challenges

Let us talk about some interprofessional workflow challenges, and I would like to trigger you to think about this as we review some cases here in just a second.

Think about patients that you care for. Who owns initiation for medications? Is it primary care? Is it cardiology? Is it nephrology? Is it a team sport?

On the flip side, who are the individuals who are potentially removing therapy and paying attention to when it is time to restart therapy?

The multidisciplinary care may include pharmacists. We are really encouraged across the US about the increased use of pharmacists for GDMT initiation and intensification as really valuable members of the team. Then nurse navigators, those who are transitioning patients from inpatient to the ambulatory setting, providing education to patients about the reason for advocating for themselves to not stop their GDMT about why it is important for them to remain on these therapies.

Then using the EHR to prompt you to identify eligible patients early in their disease states, so for those who are in the community setting, really those identification tools as well as some novel tools that are coming down the pipeline, potentially utilizing AI to identify patients in large cohorts.

Integrating care with CKM. We have talked about this digital integration this week quite a bit, but think about how can it really help with CKM clinics to improve clinic efficiency. Those who know me well know that I am all for doing it right and doing it on time.

Delayed Optimization and Underuse of GDMT in HF

We talked a little bit about GDMT, as Dr. Taub reviewed. I will leave you with this slide. The big take home point is that GDMT is not only delayed, it is never initiated. It is underutilized in high-risk patients. It is our job as providers to be aware of that and help make sure that we overcome that gap.

Underuse of GDMT: It Is Not Only SGLT2 Inhibitors and HF!

It is not just SGLT2 inhibitors and heart failure that are underutilized. It is across all the classes that we just reviewed. Some of those reasons are costs, safety concerns and clinical inertia. I would beg you all to ask yourself, what is it that impacts me and my practice the most?

If I ask for a raise of hands, a lot would raise their hand because of cost. We have to acknowledge that that is a barrier. If cost becomes no longer an issue, are you there on the front lines to help make sure that patients get access to meds?

Factors Contributing to Clinical Inertia

These factors that contribute to this clinical inertia from a health system, a clinic or a hospital to an individual provider, and most importantly, to the patient are listed here. There is many factors: lack of access to guidelines, lack of awareness that these guidelines exist, which no one in this room hopefully will have that problem now, right, Dr. Taub? Time constraints. How many of you have seen patients in 15, 20 minute visits? It is quick. There is a lot to cover.

From a provider perspective, it is just overall knowledge gaps, lacking confidence in measurement. Sometimes it is easier to do nothing than it is to add more therapy. Polypharmacy is a really significant barrier across the US in these populations.

It is our role and responsibility to ensure that if the patient have lack of awareness, that is on us to help overcome that. Health literacy is very challenging. Ensuring that your patients understand the reason for the decisions that you are making. Or a patient who does not have symptoms, it is hard to convince someone who is feeling well that we need to add another therapy to their regimen.

Most importantly, and this is something that nurses and APPs can really help with, is lacking confidence in the healthcare provider's team who are not working together or not working collaboratively.

Patient Barriers in CKM Syndrome Management

If we keep the patient at the center of all that we do, when we look at financial costs, access to care, including transportation, all of the interdisciplinary team members who need to see the patients, how much insurance costs, what the medications are and hospitalization and outpatient appointments.

There are a number of factors that are going into patient barriers. We will not fix them all, but it really is important to recognize and be aware of which of those factors are impacting each of your patient.

Consequences of GDMT Underuse

If we underutilize GDMT, of course, this group all knows this. More patients die, more patients have a delay in disease progression, and we miss that earlier intervention window. What was it yesterday, $800 billion in heart failure estimated costs within the next 10 years. That is incredible. It is really important for us to think about how we are impacting overall healthcare costs here, not only in the US but across the world.

Strategies for Better GDMT Care

Some strategies. You will have these slides. Please download these and use these. Overcoming clinical inertia, peer resistance with guideline evidence, navigating insurance barriers. Talk about those in your group as we review some of these cases together.

I will pass it over to Dr. Taub, who is going to talk to us about the next topic.

Connecting the Evidence to Action: Nurse-Led Strategies For Using GDMT to Improve Outcomes

Get Ready to Interact

Dr. Taub: The next section is going to be interactive. We are going to start with a short patient video. It is an AI-generated patient. Then we are going to walk around and have you discuss at your table the case. Stephanie and I will walk around and participate in some of those discussions. Then we will have a polling question and then we will end with what are the takeaways from the case.

What we are really hoping for is a lot of interaction at your tables and some good questions from the case for us.

AI Patient Robert: 68-Yr-old Male, “I am doing fine, why change anything?”

We are going to start with Robert, who is a 68-year-old male, who feels like he doing fine and why change anything in his medical regimen?

Robert: Hi. Yes, I just got out of the hospital a couple weeks ago. They said my heart is weaker than it should be. Something about heart failure. Honestly, I feel okay right now. I mean, I get a little tired walking to the mailbox, but that has been going on for a while. Nothing new. They already changed a couple of my meds in the hospital. I am taking them like they told me. I just do not really want to add more pills unless I have to.

My primary doctor said we would keep an eye on things and maybe adjust later. I like that plan. I have also got diabetes and some kidney issues, so I do not want to mess anything up by adding new medications. I have heard some of these heart drugs can affect your kidneys. To be honest, it is already a lot to keep track of.

If I am feeling okay, is it really necessary to change anything right now?

Dr. Taub: Typical patient. We get this all the time.

Let's Discuss: Robert (68-Yr-old Male) Who says He is Doing Fine

In your groups, we would like you to discuss Robert's story and think about do you see patients like Robert and what has gone well with Robert's care and what can we improve upon? Stephanie and I are going to be walking around and listening to your dialogue.

Dr. Barnes: I am hoping he is on the right stuff.

Dr. Taub: We hope so. Right?

Dr. Barnes: We have got some questions from the online audience too, which is great.

Dr. Taub: Yes, this was a great discussion. Stephanie, what were the things that you were hearing at the tables?

Dr. Barnes: I heard one of the tables say patients like Robert, I want to be supportive of, and I really would like to make sure that he knows that we understand and acknowledge. We are going to continue this presentation for this patient. We would like to talk to you.

Dr. Taub: I know you guys have had such great discussions, and I know you want to continue it, but we will have another case where you can have more discussion. We are going to move on. Stephanie, what did you hear?

Dr. Barnes: Yes. One of the tables was talking about is trying to acknowledge Robert's request and being respectful of this patient's request to minimize the therapy but having a standard script that is used when you have someone like Robert who is averse to adding therapies. Think of a script that you can use and get one that you are comfortable with. Practice it in the mirror in the morning.

Poll 3

Dr. Taub: Let us do our question around Robert’s case. He is a 68-year-old male with recent heart failure hospitalization, type 2 diabetes, CKD stage II. He feels he is stable and prefers to have no medication changes. He is on a low-dose ACE inhibitor and beta-blocker. What is the most appropriate next step to optimize care? I already heard dialogue about this at the tables. Would you:

1. Avoid therapy changes due to concern about his kidney function and safety;
2. Continue his current therapy and re-assess symptom and risk at a later visit; or
3. Defer GDMT adjustments to his primary care provider for follow-up management; or
4. Initiate additional GDMT with a structured monitoring and follow-up plan?

That was what I heard when I was walking around. This is a really fantastic audience.

Key Takeaways and Addressing Robert’s Case

You already got the key takeaway messages from this case, which is just because somebody feels okay at the moment, it does not mean that they are stable. It does not mean sub-clinically everything is going well and that they are optimized. Early GDMT is really important in terms of preventing repeat hospitalization.

I already heard you say at the table some of the things that you would say to Robert. One of the key takeaways from my listening in is all of you emphasized really good communication, education, both of Robert, his family members and also the other providers like the primary care provider.

Any additional thoughts, Stephanie?

Dr. Barnes: I cannot underscore enough the importance of nurse-led support to help with addressing the clinical urgency in Robert's case, and the risk of omission for him, and normalizing that treatment escalation as a standard and expected care could be really helpful.

Dr. Taub: Are there any questions that we want to answer?

Dr. Barnes: There is a great question online. Actually, the bottom question. Difference between CKM and cardiorenal and patients may hear both of those terms used. Your thoughts on that?

Dr. Taub: Cardiorenal was an older term, which was really talking about the interaction between the heart and the kidneys, especially in the context of heart failure. Sometimes we would see somebody come in for a heart failure exacerbation, and their kidney function would go up and we would say, “Oh, that is cardiorenal.”

Now we have gotten more sophisticated and we have a broader term to encompass that interaction. That is CKM. We are also acknowledging as part of CKM, it is not just the heart and the kidneys that are impacted, but there is other systems involved, including the endocrine system. One of the things that we sometimes are forgetting is the liver.

A lot of these patients, for instance, with heart failure, with preserved ejection fraction, have MASLD and that eventually progresses to fibrosis and MASH. It is a much broader way of really talking about this interaction between the multiple organs.

Why do not we go to the next case?

From Treatment Hesitation to Confident Follow-Through  

Dr. Barnes: We have a next case from treatment hesitation through confident follow through. I would like you to meet my friend Angela.

AI Patient Angela: 62-Yr-Old Female, “I am worried about side effects.”

Angela is worried about side effects from medications. Angela, take it away.

Angela: I picked up the new prescriptions, but I have not started them yet. I did some reading online and, honestly, it scared me. One of them said it could cause urinary infections. With my diabetes, I already worry about that.

The other one, it can raise potassium. My kidneys are not great already, so that does not sound good. I just do not want to end up back in the hospital because of a side effect from something that is supposed to help me. I feel like I have been managing okay so far. Maybe not perfect, but stable. Is it really worth the risk to add these medications?

Dr. Barnes: Similar to that last case, let us discuss among ourselves if we have time. Do you have some time for discussion for this case? Okay, great. Talk about Angela. What do you would you do in your case? How would you approach this and what questions would you have? We will walk around just like we did before.

Great conversations. You have got your post-test questions. We will close up this conversation, and we would like for you to go ahead and answer the fourth polling question. Go ahead and vote.

Poll 4

We have Angela, 62-year-old with heart failure, type 2 diabetes and CKD stage III. She was prescribed an SGLT2 inhibitor and MRA did not start them because she was concerned about urinary infections, hyperkalemia, and kidney function. Would you:

1. Delay initiation and revisit therapy after additional evaluation;
2. Initiate one medication first to reduce perceived risk and assess tolerance;
3. Initiate prescribed therapies with clear education on risks, benefit and monitoring; or
4. Refer back to the prescribing healthcare provider to address concerns before you start therapy.

Great. Majority in this room would initiate prescribed therapies educating on risks, benefits and monitoring. There was about 17% initiated one med first to reduce perceived risk and assess tolerance. Good response there. Majority answered that one the way that we would.

Key Takeaways and Addressing Angela’s Case

Some key takeaways in addressing Angela's case. Dr. Taub, what did you hear as you were walking around for key takeaways for Angela's case?

Dr. Taub: I heard from across the tables about just educating patients on what the potential side effects are and strategies for mitigating side effects, and also clear communication so that patients are aware that they can contact us and we can walk them through the side effects that they do not have to suffer.

Dr. Barnes: Fantastic. Same with my group. Some key vernacular that you could say to Angela is that validating concerns, ensuring that you are a trusted member of the team, that you will continue to follow. One of the groups that I rounded on said, we have got this standard education that we are providing to patients that address just these questions.

Not just disease state education, but if this is your concern, this is how we can respond. As a nurse-led action, acknowledging and validating the patient's concerns, but guiding them toward what we know will help improve their quality of life and their quality of life is very important.

Posttest Assessment  

Posttest 1

Let us go to our post-test assessment. We will start with our first question, which is going back to that 66-year-old woman with type 2 diabetes, hypertension, obesity, CKD stage III and six months of progressive fatigue and decreased exercise tolerance with a mildly elevated NT-proBNP, a normal ejection fraction of 55%, mild left atrial enlargement and grade 1 diastolic dysfunction. What is the most appropriate next step? Are you going to:

1. Continue monitoring;
2. Treat symptoms of CKD and repeat echo in 12 months;
3. Apply a structured HFpEF approach and reassess volume status, and that includes using some of the risk scores we talked about; or
4. Intensifying antihypertensive therapy and reassessing in four weeks.

Posttest 1

The correct answer is C. When we look at the pre and the post. You guys were already so on top of it pre. We did increase it from 75% to 92%. We want to be utilizing some of the risk calculators, those scores that we talked about and just helping us stratify whether a person is at high-risk for developing heart failure. Most of you got that one.

Posttest 2

Let us go to the next question. A 70-year-old man with HFrEF, type 2 diabetes, CKD stage III is seen one week after hospital discharge on a low-dose ACE and beta-blocker. He feels about the same and is worried about worsening kidney function with additional medications. Which of the following is the most appropriate next step? Is it:

1. Initiate additional GDMT with patient counselling and a structured monitoring plan;
2. Initiate one additional GDMT and defer others until renal function stability is confirmed; or
3. Prioritize symptom stability and defer further GDMT intensification; or
4. Slowly uptitrate current medications before introducing additional GDMT.

Wow, this is an incredible audience. You guys already understood this concept before, and then we got 100% of you to say the correct answer, which is A, initiate additional GDMT.

Posttest 2: Rationale

The case is also exemplified how important it is to initiate additional GDMT.

Posttest 3

Okay. A 69-year-old patient with HFrEF, type 2 diabetes, CKD stage III, started GDMT two weeks ago, is on SGLT2, ACE, beta-blocker, MRA and loop diuretic. At follow-up is light-headed but has stable labs and no dyspnea or edema. What is the most appropriate next step? Would you:

1. Stop the SGLT2;
2. Reduce or hold the loop diuretic;
3. Stop the MRA; or
4. Make no changes.

Interesting. 91% got it correct pre. Then it went down to 88%. Some of you went to SGLT2 to stop the SGLT2 and to stop the MRA.

Posttest 3: Rationale

If you look at this patient, the creatinine is stable and the potassium is also within normal range. You do not need to stop the MRA. In terms of the hypotension, I understand why some people would pick SGLT2, but the SGLT2 is the most evidence-based in terms of preventing heart failure readmissions. The diuretic is what you can reduce, and that will help with the blood pressure.

Q&A

We have some time. We have three minutes for questions. Let me go through them really quickly. How do we best communicate not stopping heart failure GDMT when there are small increases in creatinine, when we know that therapies do this?

I will start and I will have you follow-up. I counsel patients when I start GDMT that you are going to see an increase in creatinine. That is actually good. It means that the therapies are working. I always tell people not to worry about increase in creatinine with initiation of GDMT and it is expected.

If you give patients that counselling, then they are not as worried. To tag on to that, the second part of that question is, how do you deal with trust issues when a different clinician has advised differently?

I would say be proactive about the documentation in your notes with the rationale that the patient had these questions and the response that you gave them, and close the loop, if possible, with that external other team member to ensure that they know the rationale for your decision-making. This is a team sport and you are here learning and lead the way so you can help teach others.

Also a lot of different providers have different tolerance for what they feel comfortable with. Primary care provider may feel less comfortable, say, with a cardiologist. So that closed loop communication can really help.

Then someone from the virtual audience asked, using the CVD plus risk estimator, the BMI cannot be above 39, making it difficult for me to use this resource. Any suggestions for another app?

I would say this is a case where do not over-rely on these risk estimators. When you see someone with a BMI of 39, that is an incredibly high-risk patient and they have a lot of other comorbidities just with that elevated BMI alone. So you do not really need a risk calculator here to tell you that this person is incredibly high risk. I do not know if you do this, but sometimes if those calculators exceed the highest risk, I will put what the highest value is to give me a comfortable response.

A lot of those calculators include interpreted responses at the bottoms with scripts that can be very helpful. But great answer to that one.

Go Online for More Coverage of HF and CKM!

If there is anybody from the audience that has a question that we did not answer, please ask. We have time for one more question.

Speaker: In my practice, because otherwise [inaudible] I really took longer to follow-up with that because I know there is going to be that initial increase in creatinine over time [inaudible]. I know all the guidelines tell you and all of the recommendations are new labs. We always do labs at 22 weeks. Should we be extending that time between labs? I mean, I have never seen a crazy increase, but I know that can happen. What is the best action for that? Do we do too many labs?

Dr. Taub: I can start by saying it depends on what you are starting. I mean, definitely if you are initiating an SGLT2 inhibitor, you can wait six weeks. You can wait three months to do the next set of labs. The only time you want to check them a little bit earlier is if someone already has CKD and you are initiating an MRA. This is where you are really looking at the potassium and you counsel the patient. There might be an increase in creatinine, but that is part of the natural course of how this drug works. There is an initial increase and then there will be a dip.

Dr. Barnes: It is that counselling. To be on that one week time frame though to your point, really beyond that one week, if things look great, one to two weeks, we are done.