It really is a pleasure for me to spend a little bit of time with you and talk about worsening symptoms and hospitalization for heart failure.
So, our objectives today will be to discuss hospitalization as a pivotal point in the clinical trajectory of heart failure. And I like to look at hospitalization for heart failure as being a learning moment for the clinician. It’s an opportunity for us to learn much about our patients, and why they become decompensated, and how we might alter their clinical outcome. And it’s also a teachable moment for the patient; it’s an opportunity for us to educate patients and to impress upon them the importance of adherence to their medical therapies. In that regard, we’ll highlight some strategies for improvement and optimization of treatment plan for patients with heart failure, and we’ll provide practical guidance for identifying predictors of worsening heart failure and educating on the importance of patients’ self-management.
So, I suspect that all of you have seen a graphic that looks something like this, or perhaps this one previously. This has circulated for many years, and demonstrates the natural history of heart failure, underscoring the fact that heart failure is a progressive disease, involving chronic decline of cardiac function and health-related quality of life, and then ultimately resulting in high rates or high risk of morbidity and mortality. And what you see along this natural history or clinical trajectory of heart failure is that it is periodically punctuated by episodes of decompensation, or worsening heart failure, requiring hospitalization. And the other thing that you’ll notice here, is that with each one of those decompensation events, the patient tends to come out on the back side a little bit worse off than they went into it. And this is the trajectory that we ultimately like to—like to alter, either by keeping patients out of the hospital or discharging patients from the hospital in better shape.
So, hospitalization for heart failure is common, if you look at the heart failure population, and this is regardless of LV ejection fraction. This is for HFrEF patients, HFpEF patients, and if you come from Europe, for HFmrEF patients, that in-between group of patients with mildly reduced ejection fractions. Over a 5-year period of time, about 80% or greater than 80% of heart failure patients will have at least one hospitalization, and many of these patients, in fact, as you know, will have multiple hospitalizations.
Prior hospitalization for heart failure increases the risk of cardiovascular death or hospitalization, and again, this is independent of LV ejection fraction. While you can see here the HFrEF population shown in blue and the HFpEF patients shown in red, and there is a higher rate of morbidity and mortality in the HFrEF patients, there is still a significant risk in the HFpEF patients.
And you can see that those patients—regardless of ejection fraction— HFrEF, HFpEF—have a significantly greater likelihood of cardiovascular death or heart failure hospitalization if they have had a prior heart failure hospitalization. So, this really provides some evidence, and it speaks to that earlier slide that I shared with you on the clinical trajectory of heart failure, and how heart failure hospitalization marks a significant event in the life of the heart failure patient and is associated with worse outcomes, increased risk of future morbidity, and mortality.
When we look at what these patients look like, at the time of presentation, at the time of hospitalization, the signs and symptoms are similar in both HFrEF and HFpEF patients. And what I’d like to summarize with this slide is the fact that heart failure patients are generally admitted because of congestion. What do I mean by congestion? I think you know that, but—you know, this is retention of salt and water, accumulation of fluid, an excess of total body fluid volume that results in pulmonary and peripheral edema (we’ll call that “clinical congestion”), and patients present with symptoms such as dyspnea on exertion, peripheral edema, pulmonary crackles, maybe even dyspnea at rest or paroxysmal nocturnal dyspnea or worsening orthopnea. These patients are generally congested; they’re wet. They’re going to require treatment for their volume overload in the hospital, and then other strategies to try to prevent the re-accumulation of this congestion, in the ending days of their hospitalization, and as outpatients.
There are also specific precipitants of heart failure hospitalization which are associated with variable mortality risk. Now, it turns out that the vast majority of patients who are admitted to the hospital with decompensated heart failure don’t have ischemia or an ACS, but if they do, it is associated with a substantial increase in risk for mortality.
So, if a patient is admitted to the hospital for worsening heart failure with a concomitant acute coronary syndrome, you’ve got to think about addressing the coronary artery disease, the ischemic heart disease. Now, that said, I want to mention one caveat. I think, as many of you also know, the majority of heart failure patients at the time of admission to the hospital will have an elevated troponin level. If you do a high-sensitivity troponin measurement, you’ll see a measurable troponin level in about 90% of patients with decompensated heart failure. Those are not all ACS patients; you have to distinguish between a troponin increase related to decompensation of heart failure alone versus that associated with an acute coronary syndrome. But it’s a very important part of the investigation, because as you can see, a concomitant acute coronary syndrome has significant implications for a clinical outcome.
Persistent signs and/or symptoms of heart failure should prompt further investigation. I already addressed some of these, but again, regardless of ejection fraction, we need to think about the patients’ comorbidities. This is personalized care, personalized management, of the heart failure patient. Does the patient have underlying coronary disease? Might ischemia or an acute coronary syndrome be playing a role here? Do they have heart failure? Has their rate become less well-controlled? Or do they have a new onset of an arrythmia that has contributed to their decompensation? And so on and so forth. We’ve talked about a lot of these comorbidities already and contributing factors, so I won’t reiterate all of them, for time’s sake, but I think the key point here is that we not only want to focus narrowly on treating the decompensated heart failure but look at the patient in a holistic way and try to understand the factor or factors, the comorbidities that are leading to their worsening heart failure, evaluate them, and adjust those, as well.
Well, what do the guidelines tell us about biomarkers? BNP or NT-proBNP are playing an increasingly important role in the evaluation and management of the patient with decompensated heart failure. I think you all know that in the setting of chronic heart failure, in the outpatient setting, that BNP is an important prognostic indicator, and some people have attempted to use it as a means to guide chronic heart failure therapy with mixed results. And in the emergency department, it’s used as a diagnostic tool for trying to differentiate worsening heart failure from other causes of shortness of breath, such as COPD exacerbation or bronchitis or pneumonia. But in the setting of decompensated heart failure, there are really two important things that we know about the use of the measurement of BNP.
First of all, the baseline measurement of BNP, at the time of hospitalization for decompensated heart failure, is an important measure of clinical outcomes—acute clinical outcomes in these hospitalized patients with worsening or decompensated heart failure. And secondly, we know that a change in BNP during treatment of that heart failure in the hospital also has a meaningful value in predicting outcomes in our patients. And I’ll show you some data for that on the next slide.
And there’s a number that I want you to remember here, and it is a 30% reduction in BNP during hospitalization for heart failure. If you can achieve that 30% or greater reduction in NT- proBNP from the time of admission to the time of discharge, your patient’s prognosis is better. So, this is why the guidelines shown on the prior slide encourage us with a relatively high level of recommendation, a class 1 recommendation for baseline assessment of NT-proBNP, a class 2a recommendation for the subsequent measurement of BNP or NT-proBNP prior to discharge, because it turns out that the information is highly informative.
So, this biomarker has proven to be useful in the evaluation of treatment of patients in the hospital with decompensated heart failure.
Also of note, natriuretic peptides are prognostic, regardless of the LV ejection fraction. And again, we’re coming back to a common theme here, that when it comes to decompensated heart failure in the hospital, don’t think about ejection fraction; this really is sort of a common, final pathway for heart failure patients, regardless of ejection fraction, and the good news is that the evaluation and some of the tools, such as BNP, that we have to better understand prognosis and outcome in these patients are useful tools in both HFrEF and in HFpEF patients.
Also important to note that prior hospitalization for heart failure does have an impact on symptom burden and heart-related quality of life.
The data shown on this slide looks particularly at the Minnesota Living with Heart Failure quality of life questionnaire. Remember that with that questionnaire, a higher number is a worse number. You know, in most things, if you score higher, you’re doing better. But with this quality of life questionnaire, a lower number means a better quality of life, a higher number means a worse quality of life.
And if you look at patients with prior heart failure hospitalization, or with certain symptoms on presentation, such as angina or paroxysmal nocturnal dyspnea, or dyspnea at rest, the presence of any of those is associated with a worse quality of life.
So, let’s talk about the goals of hospitalization. These focus on intermediate- and long-term care needs. You know, of course, there are a couple of short-term or intermediate-term goals. I told you at the outset that the majority of these patients are congested at the time of admission. So, of course, one of the major goals of treating decompensated heart failure is decongestion.
And there are plenty of studies, both registries and controlled clinical trials, that demonstrate that we are discharging a high proportion of our heart failure patients from the hospital with residual congestion. Studies show that anywhere from a third to a half of our heart failure patients at the time of discharge have evidence of residual congestion. Inadequate weight loss, signs or symptoms of pulmonary and peripheral edema, and so on and so forth. And it is now very clear that patients discharged with residual congestion are at higher risk for readmission, and—and mortality. So, decongestion is at the top of the list. You have to focus on getting patients as dry as you possibly can. And while we worry about worsening renal function in these patients— and during the treatment of their heart failure in the hospitalization—you know, current thinking is that if you have to bump the creatinine a little bit, to get the patient more adequately decongested, that that is an acceptable goal, because it is the decongestion, perhaps a bit more than the worsening renal function, that will determine their risk for readmission. So, I can’t emphasize enough the importance of this goal of decongestion.
We want to initiate, titrate, and/or optimize guideline-directed medical therapies while patients are in the hospital. And this had been a real paradigm shift over the past two decades.
You know, we used to treat acute decompensated heart failure as a separate entity, and then we would begin to implement those chronic outpatient heart failure strategies after the patient came back to the outpatient clinic. But we’ve now learned that it makes sense, it’s safe, and in fact, because it is a teachable moment, patients’ adherence rates to guideline-directed medical therapies when started in the hospital are higher. So, this is a beautiful time to not only decongest the patient and address their acute decompensation, but also get them started on a guideline-directed medical plan that will alter their long-term outcomes as well.
In-hospital clinical trajectories can be identified with a thorough evaluation, and I’m going to refer you to—if you haven’t seen it yet—the paper that’s referenced here. This is Hollenberg, et al, published in JACC So, you know, this is designed to review, recommend a practical approach to implementing heart failure guidelines for the patient with decompensated heart failure. And it provides a wonderful roadmap; I really—I really love this paper, and I would really highly recommend it to you. And it talks about the inpatient trajectories of heart failure treatment. I mean, this is a pragmatic understanding of what happens to these patients and how to address it. So, the determinants of the clinical trajectory in the hospital include patient symptoms, clinical signs, laboratory markers, and imaging, if completed—the presence or absence of complications, the assessment and treatment of comorbidities, and treatment alignment with the goals of care.
And when you read this paper, you will see that the authors suggest that there really are three main trajectories, and as you get into that first 24-48 hours of treatment of the patient with decompensated heart failure, you should do a trajectory check. A group of patients are improving towards their target. These patients do exceedingly well. You give them a little bit if diuretic, they diurese, they’re getting decongested, their kidney function is stable or improving. Everything about them seems to be going well. Then there’s a second group of patients. This is the group of patients that initially improved, but now their progress has stalled. You know, we see this all the time. We give a patient some IV diuretic, and they start to make a lot of urine, and we’re feeling pretty good about things, and we come back and round the next day, and they tell us their symptoms are no better. On exam, they’re still congested, and maybe their renal function is starting to worsen a bit and they’re beginning to develop some diuretic resistance. And then finally, and perhaps most concerning, is the third group of patients. The group of patients that’s not improved, never improved from, you know, the moment you’ve begun to treat them, and in fact, is demonstrating in-hospital worsening of their heart failure. This group of patients tends to have a bad prognosis.
And this pragmatic paper on how to address a decompensated heart failure patient, goes on to recommend some approaches. Again, in that group of patients who’s improving towards target, just continue toward decongestion, and if on track to reach decongestion, consider in- hospital optimization of guideline-directed medical therapy for chronic heart failure. In those patients who may have initially improved but now stalled or are worsening, you need to reevaluate their current therapy, consider additional diagnoses. Is there something else going on here, that’s complicating the ADHF picture, or something that we’ve missed in the story? Consider invasive hemodynamic assessment.
So, we continue toward decongestion and we optimize GDMT in these patients who are improving towards target. Decongestion, GDMT, address their comorbidities, and again, address the goals of care and educate the patient.
Heart failure management is multifactorial. I have to admit, sometimes as a physician, I get so focused on the medical therapies—the guideline-directed heart failure therapies, the guideline- directed device therapies, or in advanced heart failure, thinking about advanced therapies— you know, that sometimes I may not get enough—give enough attention to the lifestyle changes and patient education, and addressing some of those socioeconomic barriers are important as well.
You know, talking about weight loss and smoking cessation, cardiac rehab, medication adherence, and so on and so forth.
And then transition to a maintenance guideline-directed medical therapy. You can see that if you start a GDMT in the hospital, patients do better. Outcomes are improved. Focus on the table here on the right-hand side. So, starting any therapy versus no therapy, you see a significant reduction in both HFrEF and HFpEF. About a 30 to 50 percent reduction in improvement and outcome. If, on the other hand, you discontinue any therapy versus maintaining therapy, you have a worsening of clinical outcome.
And how often do we do this in hospitalized patients with ADHF, right? The patient comes in, they’re a little bit hypotensive, we stop their ACE inhibitor, or we stop their beta blocker, or we decrease the doses, and then we send them out. You know, on less stuff. Right? As a heart failure specialist, it’s the bane of my existence, because I work really hard; sometimes I take 6 months to get patients on optimized GDMT, and then they get hospitalized once and everything gets stopped and I have to start all over again. So, we want to try not to do this.
Well, we’re not doing a very good job of it right now. If you look at the initiation of GDMT at discharge in hospitalized patients with ADHF, you know, you’ll see that it’s not very good. Ten or twenty percent of patients go home, you know, with some initiation of GDMT. We’ve got to do better than this. Okay.
Well, what about those patients who stall in reaching their decongestion goals? Well, as mentioned, we have to evaluate the current therapy. We may intensify the diuretic regimen and consider alternative therapies, including IV vasoactive medications. Consider again comorbidities. We may consider that invasive hemodynamic assessment.
So, I am going to move to some of these symptom perception and self-care issues and strategies, because I do think this is very important. We’ve got to address all of the socioeconomic, as well as patient and condition and therapy-related items here.
So, we want to capitalize on this opportunity in the hospital, when patients are most disposed to adherence. We want to address the socioeconomic and health system issues, cost, lack of access, lack of support, poor communication. Right? We have an early postdischarge heart failure clinic. We schedule every patient for a visit within 7 to 10 days postdischarge. About 50% of them show up. Why? Because they don’t have transportation, they can’t afford to come. Getting into the big city is difficult. Maybe the follow-up has been communicated poorly to them, or maybe they went home and weren’t even able to fill their prescriptions, because they couldn’t afford doing it. So, these are—these are really huge problems that need to be addressed.
So, in conclusion, hospitalization is a pivotal point in the clinical trajectory of heart failure and is an event with considerable prognostic impact in both HFrEF and HFpEF patients. The in- hospital clinical trajectory of patients determines immediate and long-term care. Decongestion and assessment and optimization of guideline-directed medical care are key goals for our hospitalized patients. We want these patients to leave the hospital better off, rather than worse off, compared to when they were admitted to the hospital. And that goes for the initiation of guideline-directed medical therapy, as well. Multiple precipitants can trigger periods of decompensation that necessitate hospitalization, so identification and treatment of those precipitants is important. Close monitoring of worsening heart failure and early recognition of symptoms is key in mitigating adverse outcomes, and hospitalization provides an opportunity—and I’m going to say this again— an opportunity for both the clinician and the patient, to address barriers to care and adherence, as well as to optimize therapy. So, with that, I will conclude my formal comments.