The Progressive Nature of Heart Failure

EP: 1.Heart Failure Clinical and Economic Burden

Now Viewing

EP: 2.The Progressive Nature of Heart Failure

EP: 3.Link Between LVEF, NT-ProBNP and Cardiac Remodeling

EP: 4.Improved Understanding of Heart Failure

EP: 5.Treatment Goals for Patients With Heart Failure

EP: 6.The HFrEF Standard of Care

EP: 7.Heart Failure Management Unmet Needs

EP: 8.Utilization Management Strategies for Appropriate Treatment

EP: 9.Challenges in the Management of HFpEF

EP: 10.Differences in Standard of Care: HFpEF vs HFrEF

EP: 11.Ensuring Timely and Appropriate Access to Therapy

EP: 12.Differences in Economic Burden: HFpEF and HFrEF

EP: 13.PROVE-HF Trial Overview

EP: 14.PARAGON-HF Trial Overview

EP: 15.Recent Findings from the PARALLAX Study

EP: 16.Promising Findings From the TOPCAT Study

EP: 17.Differences in Leading Treatments for Heart Failure

EP: 18.When to Add an SGLT2 Inhibitor to Treatment Regimen

EP: 19.Heart Failure Sites of Care

EP: 20.How Approved Agents Will Change the Standard of Care

EP: 21.Heart Failure Management During COVID-19

Scott D. Solomon, MD: When we talk about heart failure, we need to think about whether we’re talking about heart failure with reduced ejection fraction, for which we have clear guideline-directed therapies, or heart failure with preserved ejection fraction, for which we don’t have clear guideline-directed therapies. The basic principles of heart failure are similar for both HFrEF [heart failure–reduced ejection fraction] and heart failure with preserved ejection fraction in that all these patients have elevation in intracardiac pressures. In fact, a great definition of heart failure that I like is that it is an inability to supply enough cardiac output to the body or to do so only in the setting of elevated filling pressures. When we think about it that way, we realize that the primary goal of treatment of heart failure is generally to relieve congestion. In patients with severe left ventricular dysfunction and low output heart failure, we do a lot of things to try to increase their cardiac output. I’m going to focus primarily on the more chronic types of heart failure, where the biggest problem for our patients is congestion. For those patients, we treat them with therapies that relieve congestion, like diuretic therapies.

How do we monitor this? The tried-and-true way to monitor heart failure progression is with physical examination and taking a history because patients will tell you if they are having progressive shortness of breath. They realize that weeks or months ago, they could do certain things that they can’t do now without getting short of breath. That’s an extremely important part of your diagnostic armamentarium as physicians. We will also assess various things that give us an indication of whether a patient has volume overload. For example, we’ll look at their jugular veins, and we’ll look at their lower extremities to see if there are edemas. Patients sometimes have edema that extends beyond the lower extremities. We ask our patients to follow their weights. We listen to their lungs for evidence, for example, of crackles. These are all ways that we can use both the patient’s history and the physical exam to determine whether they are having progression of heart failure.

There are other symptoms that patients have that are more nonspecific, like fatigue, for example. My patients will sometimes simply say that they are feeling more tired, and that might be an indication that they are progressing in their heart failure. This may be after the physical exam and history that we’re going to take and perform on all our patients. Although to be frank, it’s a bit harder in the setting of COVID-19 [coronavirus disease 2019] to do physical exams on our patients, so we’ve been seeing them virtually and relying more on the history and their own assessment of what’s happening in their body, such as whether they are having an edema in their lower extremities. Most patients can’t check out their neck veins but can weigh themselves and provide that information back to the physician. They can take their blood pressure and their pulse. These are all important components. Once we get beyond history and physical exam, we think about laboratory assessments to determine progression of heart failure.

We’ll start with the basics. Generally, our basic metabolic panel can give us some clues. If we have a reduction in serum sodium, this is common in patients with more severe heart failure. It also happens because of diuretics, for example, so we have to interpret these data carefully. We obviously like to know what the serum, potassium, and creatine are for our patients with heart failure because that dictates the kinds of medicines we can use.

In addition, we use specialized laboratory markers like natriuretic peptides. Natriuretic peptides [BNP] come in 2 main forms, either NT-proBNP [B-terminal pro B-type natriuretic peptide], which stands for internal pro-BNP or BNP. Whichever you use depends on what lab you’re using and what your hospital or your laboratory has for a test. Most have 1 or the other: BNP or NT-proBNP, but not necessarily both. These can be helpful in distinguishing heart failure from other entities that cause similar signs and symptoms. That’s particularly true in heart failure with preserved ejection fraction, where it can be challenging to make the diagnosis. So we would often obtain natriuretic peptide at these levels, which are different. NT-proBNP and BNP can often tell us whether a patient is having evidence of increased filling pressure. These are markers that go up in the setting of increased wall stress in the heart. In addition to natriuretic peptides, we can use high-sensitivity troponin because we know that those are elevated in patients with heart failure too. We’re used to thinking about troponin in the setting of cardiac ischemia, but they can be elevated even in patients without any evidence of cardiac ischemia just because of the increase in pulse stress.

We also do cardiac imaging in our patients with heart failure. Echocardiography makes the single most utilized imaging modality for patients with heart failure, and we do that for a number of reasons. The first is to assess left ventricular function. Ejection fraction is the metric we typically use for that. This helps us determine whether a patient has heart failure with reduced vs preserved ejection fraction. Why is that important? In heart failure with reduced ejection fraction, we do have evidence-based therapies; in heart failure with preserved ejection fraction, we don’t. Making that distinction is key. It gives us a lot of other information as well. For example, we can look at ventricular volumes. We can look at the left atrium to see if there is evidence of left atrial enlargement. We can look at the right ventricle to see if there is evidence of right ventricular enlargement or dysfunction. We can look at pulmonary pressures. We can look at the valves to determine if there’s mitral regurgitation, for example.

In summary, how do we follow progression? How do we make the diagnosis in patients with heart failure? How do we look at heart failure progression? We start with the basics: a physical exam and history, and then we go to basic laboratory values and then cardiac imaging. That composes the majority of what we do to both diagnose heart failure and follow patients with heart failure.