Hello, my name is Sandy McCrary. I'm a PA at Cardiovascular Associates in Kingsport, Tennessee. I'm the Clinical Director of Heart Success, which is the heart failure program offered by Cardiovascular Associates. I've worked in cardiology for 25 years, and today we're going to be looking at an introduction to heart failure. We're going to be looking at the definition of heart failure, reviewing the classifications and phenotypes according to the left ventricular ejection fraction. We'll also review the mechanisms and epidemiology of heart failure. We'll discuss the initial assessment and testing, as well as non-pharmacologic interventions. The reference that we use throughout the presentation is from 2022 AHA ACC Heart Failure Society of America Guidelines. You have a link to that here, and this is an excellent document to have either available electronically or a hard copy because it takes the whole discussion of heart failure from the very beginning with pre-heart failure all the way through advanced heart failure and discusses treatments, considerations, testings, and it's just an excellent reference to have. What is heart failure? It seems like a very simple question, but the answer is a little bit more complex. Heart failure is a clinical syndrome that's caused by an impairment of the ventricular filling or the ejection of blood. It results in the inability of the heart to provide adequate perfusion to the tissues while maintaining normal cardiac filling pressures. Heart failure is associated with a variety of interrelated structural, functional, and neuro-hormonal alterations that can be both beneficial as well as maladaptive. Heart failure is not synonymous with cardiomyopathy or with left ventricular dysfunction. In fact, it's associated with a wide spectrum of LV functional abnormalities. There can be a normal LV size with a preserved ejection fraction, or there can be severe dilatation and a markedly reduced ejection fraction. I've listed here quite a few abbreviations and acronyms that we'll be using throughout the presentation. So this is here for your reference. So let's look at heart failure. What does heart failure mean? How do we determine a diagnosis of heart failure, and how do we evaluate a specific patient that has heart failure? First, we'll look at the Framingham classification of heart failure. This is based on concurrent presence of either two major or one major and two minor criteria. The major criteria include P and D, weight loss of more than 4.5 kilos in five days in response to treatment, JVD, RAILs, acute pulmonary edema, hepatojugular reflux, an S3 gallop, elevated central venous pressure and circulation time, radiographic cardiomegaly, pulmonary edema, visceral congestion. The minor criteria, and these can only be considered if the minor criteria cannot be attributed to another medical condition. But the minor criteria include nocturnal cough, dyspnea on ordinary exertion, decrease in vital capacity, pleural effusion, tachycardia, hepatomegaly, and bilateral ankle edema. Another way to assess the patient with heart failure is with the NYHA functional class and the ACC AHA stages. The NYA functional class ranges from one through four and characterizes the symptoms and functional capacity of the patient. This is an independent predictor of mortality. It is a subjective assessment by a clinician, and therefore you may have a difference of opinion between two providers that assess that patient. It can change over time and the patient can move from one class to another. On the other hand, the ACC AHA stages of heart failure, which range from A through D, are based on structure and damage to the heart. This assesses the development and progression of the disease. The advanced stages and progression are associated with reduced survival. There is no moving backwards between stages. Once symptoms develop, then that patient is a stage C and stage B will never again be achieved. So let's look more specifically at the NYHA functional class. Class one is a patient who has no symptoms of heart failure. Class two is a patient who has symptoms of heart failure with moderate exertion. And this would be something like walking two blocks or climbing two flights of stairs. But they're comfortable at rest. Class three would be a patient with symptoms of heart failure with minimal exertion, such as walking one block or climbing one flight of stairs. But again, they have no symptoms at rest, but less than ordinary activity causes their heart failure symptoms. And then class four is a patient who has symptoms of heart failure at rest. Again, the NYHA class is based on symptoms alone. Therefore, it does allow movement from one class to another if a patient improves or if a patient's condition deteriorates. The stages of heart failure look at a different perspective. With the updated guidelines issued in 2022, there was specific titles placed on each stage of heart failure that are very descriptive. We have stage A, which is a patient at risk for heart failure. This patient does not have and has never had signs or symptoms of heart failure. And they do not have structural or functional heart disease or any abnormal biomarkers. But they are at risk for heart failure because they are hypertensive or they have cardiovascular disease or diabetes, obesity. They may have been exposed to cardiotoxic agents such as chemotherapy or recreational drugs. There may be a genetic variant for cardiomyopathy. They may have a family history of cardiomyopathy. So again, stage A is a patient who is at risk for developing heart failure. Stage B is a patient that is considered pre-heart failure. They likewise do not have any current or any previous signs or symptoms of heart failure. But they do have evidence of one of the following. First, they may have evidence of structural heart disease. They may have evidence of increased feeling pressures. And these can be assessed by both invasive as well as non-invasive measures. Non-invasive measures would include the natriotic peptide levels or echocardiograms. Of course, invasive measures would be information obtained through cardiac catheterization. They may also have risk factors as well as increased natriotic peptide levels or persistently elevated cardiac troponin in the absence of a competing diagnosis. And then stage C is your patient who has symptomatic heart failure. They either have symptoms currently or they have previously had signs or symptoms. Stage D is the patient who has advanced heart failure. This is your patient who has marked heart failure symptoms that in these symptoms interfere with their daily life. They may have recurrent hospitalizations despite attempts to optimize their guideline directed therapies. And then finally, we also want to classify the patient according to their ejection fraction. The initial evaluation will include the ejection fraction. Just as a reminder, normal ejection fraction is an EF of 55 to 60. So upon initial classification, if the patient is considered HEF REF or heart failure with reduced ejection fraction, that means that patient's ejection fraction is 40% or less. Old nomenclature for this was systolic heart failure, but the correct term now is heart failure with reduced ejection fraction. There's also heart failure with mildly reduced ejection fraction. This involves a patient whose EF is between 41 and 49. And this is somewhat of an update in the current guidelines because it clearly defines the folks that fall between HEF REF and HEF PEF. In the past, we weren't quite sure whether to treat them as HEF REF or to treat them as HEF PEF because they clearly had symptoms of heart failure. But now there's a more clear definition of the patient that falls between with a mildly reduced ejection fraction. And then finally, there's HEF PEF or heart failure with preserved ejection fraction. Again, in old nomenclature, this was referred to as diastolic heart failure, but the correct term now is heart failure with preserved ejection fraction. And in this situation, the ejection fraction is 50% or greater. Now, as you go through follow up with your patient and you have serial assessments of that patient or that patient has a change or a new cardiac event or are some new factor that contributes to their overall health. With the serial assessment, there may need to be a reclassification of that specific patient. For example, a patient with HEF REF may stay a patient with HEF REF, their ejection fraction may remain 40% or lower, but they may also improve. And in that situation, they're considered heart failure with improved ejection fraction. And it is very clear in the guidelines, and we'll discuss this more later on when we get to treatment. But those patients are considered improved, but that doesn't mean cured. And that means that they still need to maintain treatment for their heart failure. Heart failure with mildly reduced ejection fraction can also decline. They may have an admission with acute coronary syndrome and some event that that causes a decline in their ejection fraction. They may stay the same or they may improve. And then the HEF PEF patient also has the same possibilities as time goes on. There may be a decline in their ejection fraction for whatever reason, an ischemic event or a tachycardia mediated. They may have cancer and have to receive chemotherapy that can have an effect on the ejection fraction. Or they so they may have a reduction and fall into the HEF REF category or the HEF mildly reduced EF, or they may stay the same. So what is the prevalence of each of these types of ejection fraction levels in patients that have heart failure? Well, nearly one half of patients that have heart failure have a reduced ejection fraction, meaning, again, that their ejection fraction is less than 40 percent. Nearly one half have HEF PEF or preserved ejection fraction, and the remaining 10 to 24 percent of these patients will have heart failure with mildly reduced ejection fraction or an EF between 41 to 49 percent. So the facts and statistics about heart failure are pretty daunting. About 6.2 million adults in the U.S. have heart failure. In 2018, heart failure was mentioned in more than 379,000 death certificates, accounting for 13.4 percent of death certificates with heart failure listed as cause of death. The cost in terms of dollars is astronomical, not only for the patient and their family, but also for society. The nation had an estimated 30.7 billion dollars in heart failure cost in 2012. This includes the cost of health care services, medicines to treat for heart failure and missed days of work. The missed days of work can be for the patient, but can also be for the caregiver. And we all know that heart failure is one of the leading causes of hospitalization, and this results in about 900,000 hospitalizations in the United States each year. So why is heart failure so prevalent and why has it become even more prevalent? One reason is because of our aging population. An aging population will have an increase in cardiovascular risk factors. They also have improved survival of their cardiovascular condition. And the prevalence of heart failure is increasing globally to an estimated number of 26 million, with an additional millions of undiagnosed cases. Both the incidence and prevalence of heart failure increase steeply with age, with the average age of diagnosis being 77. Now, having said that, young patients can also have heart failure. We have patients who are in their 20s or 30s, may have a heart failure due to a postpartum cardiomyopathy or a viral cardiomyopathy. So the fact that your patient is of young age does not exclude them from the possibility of having heart failure when they present with symptoms. But certainly the incidence does increase steeply with age. Our modern therapeutics have resulted in prolonged lives of cardiac patients. Folks are living longer. And again, increasing age puts the patient at a higher risk of developing heart failure. And despite diagnostic and treatment improvements, mortality remains high. The life expectancy for congestive heart failure depends on the cause of the heart failure, its severity and other underlying medical conditions. And unfortunately, in general, only about half of all people who are diagnosed with congestive heart failure will be will survive five years and only about 30 percent will survive for 10 years. So what makes up each category of heart failure with the different phenotypes? Well, patients who have HEP REF are usually younger. They're more often male. They generally have more coronary artery disease. Patients who have HEF PEF or preserved ejection fraction are more often older, more often female and obese. And then patients that have the heart failure with mildly reduced ejection fraction fall between the other two clinical phenotypes. But they are more similar to patients with HEP REF, including a high incidence of coronary artery disease. They frequently present with comorbid conditions such as high blood pressure, CAD, atrial fibrillation, valvular disease and diabetes. So this is just a simple cartoon illustration of the heart with heart failure with preserved ejection fraction. Again, the EF is 50 percent or greater and HEF PEF results from any structural or functional impairment of the ventricular filling of blood. There is impaired ventricular relaxation. There's abnormal left ventricular filling, elevated filling pressures and an impaired response to stress such as atrial fibrillation and hypertension. This is an illustration, cartoon illustration of HEF REF or reduced ejection fraction. HEF REF results from any structural or functional impairment of the ejection of blood. There is reduced cardiac contractility and there is impaired pump function. Detecting susceptible patients very early is extremely important. And again, this goes back to the importance of identifying them early at stage A when they are pre heart failure so that we can truly make an impact and treat them as primary prevention before heart failure symptoms develop. So, of course, the initial clinical assessment, as always, goes back to our history and physical exam. The history is important because that particular patient may have a longstanding history of high blood pressure, diabetes, atrial fibrillation or obesity. They may have a history of alcohol use, which would be suggestive of an alcoholic cardiomyopathy. They may have had acute heart failure after a flu like illness, which would be suggestive of a viral cardiomyopathy. They may be having symptoms of exertional angina, which could indicate an ischemic cardiomyopathy. There may also be a family history of unexplained cardiomyopathies or amyloidosis in that particular patient. Drug use is important to determine with both recreational as well as prescription medications. Certain antiarrhythmics can be known to precipitate heart failure, as well as NSAIDs, calcium channel blockers, and of course chemotherapy for cancer treatment. In a patient who has an episode of acute pulmonary edema after they receive an infusion of blood products, or when they're post-operative from a surgical procedure, they need to be considered or suspected as possibly having heart failure because of their volume overload. So the diagnosis of heart failure can be difficult, especially in the early stages. So when we talk about symptoms, the very typical symptoms include the things we all hear about, breathlessness, shortness of breath, orthopnea, PND, reduced exercise tolerance, fatigue or tiredness, an increased amount of time that it takes for them to recover after they exercise, or ankle swelling. More specific signs of heart failure would include an elevated JBD, hepatojugular reflux, a third heart sound, laterally displaced apical impulse, or a cardiac murmur. So with initial testing in heart failure, there is no single non-invasive diagnostic test that will definitively answer if that patient has heart failure or not. It is largely a clinical diagnosis based on history, lab imaging data, as well as physical exam. We need to assess that patient's assess that patient's volume status, looking for pulmonary congestion with rails or peripheral edema, such as swelling in their legs, ascites, scrotal edema, hepatomegaly. We need to assess for elevated JBP or laterally displaced apical impulse. Also, is there an S3 present or not? Again, no single non-invasive test will give us an answer, but several testing modalities are very helpful in assessing for heart failure. Chest x-ray is one of those. On the chest x-ray, we can see if there's cardiomegaly, indications of cardiomyopathies, cephalization, curly B-lines, or pleural effusions. EKG also gives very significant information. Normal EKG makes LV dysfunction unlikely, and that's a 98% negative predictive value. If there are arrhythmias present, such as atrial fibrillation, asymptomatic PVCs, runs of non-SVT, or persistent tachycardia, that can be an indication to us regarding presence and cause of heart failure in a specific patient. There may be evidence on an EKG of ischemic heart disease. We may see evidence that there was a prior MI or an acute MI at the present time, or evidence of ischemia. LVH would indicate the patient is hypertensive. A left bundle branch block always demands evaluation when it is initially noted. So our initial testing should also include laboratory studies. A BNP or an NT-proBNP has a very high negative predictive value. For instance, if your patient presents with shortness of breath and they have a normal BNP or NT-proBNP, then that would make the diagnosis of heart failure much less likely. On the other hand, if they're presenting with shortness of breath and these levels are high, then that would indicate a possibility that their symptoms are truly due to heart failure. A troponin can indicate acute decompensated heart failure or suspected acute coronary syndrome. A CBC may point toward anemia or infection that can exacerbate a pre-existing heart failure. Electrolytes, including the calcium and magnesium, are important. Hyponatremia is an indication of severe heart failure, and this is a very poor prognostic sign. A urinalysis may show if there's proteinuria. Fasting blood sugar or hemoglobin A1c may help to indicate that that patient is diabetic. Perhaps they had no previous diagnosis of diabetes, but the lab stories may show otherwise. Elevated LFTs could suggest hepatic congestion. A lipid panel is important. Thyroid stimulating hormone level is important to obtain because hyper as well as hypothyroidism can precipitate heart failure. And finally, the test that we all rely on so much in diagnosing and assessing heart failure is an echocardiogram. The echocardiogram allows us to assess the ejection fraction. We can also see any evidence of regional wall motion abnormalities, and this may indicate the patient has coronary artery disease. We can assess the left ventricular size and function, the valvular structures and function of those valves. We can also assess for any atrial or intraventricular shunts, pericardial or pleural effusions, evidence of infiltrated cardiomyopathies. In an echocardiogram, you may have LBH and a sparkling pattern, and that can be suggestive of cardiac amyloidosis. We can also assess the diastolic function on an echocardiogram. And then our initial testing of heart failure needs to include an ischemic evaluation. And the reason is that ischemic heart disease is the underlying cause of heart failure in two-thirds of the patients who have LBH systolic dysfunction. The ischemic evaluation can be done through either non-invasive or invasive testing. The non-invasive testing can include non-invasive stress testing with imaging, and this helps us to assess for ischemic heart disease, risk stratified prognostication. We can also consider a cardiac CTA or cardiac MR. Now, these have not yet been recommended as replacement for a cardiac cath, but they are very beneficial in helping us to distinguish ischemic versus non-ischemic cardiomyopathies. Cardiac MR is also helpful to identify hypertrophic cardiomyopathy, arrhythmogenic right ventricular dysplasia or cardiomyopathy, sarcoid, amyloid, and myocarditis. Our gold standard test is cardiac catheterization. This is particularly helpful in high-risk patients to help define their coronary anatomy and is useful in patients who may be a candidate for revascularization. Patients who present with angina, positive stress test, or an unexplained cardiomyopathy may need to undergo cardiac cath. The cath gives us measurement of cardiac output as well as the degree of LV dysfunction, LV end-diastolic pressure. We can detect intracardiac shunts or anomalies as well as anomalous coronary arteries, and a right or left ventricular endomyocardial biopsy may be helpful in patients in which you need that histological diagnosis because that may influence their treatment. Examples of this would be a patient with amyloidosis or myocarditis. Now the biopsies are not routinely done because of the risk of complications, but it may be very helpful in specific populations. We can also, with cardiac catheterization, assess secondary pulmonary hypertension. Other workup to consider would be fasting transferrin saturation to rule out hemochromatosis, HIV in high-risk patients, assays to look for connective tissue disorders, pheochromocytoma, amyloidosis, and this should be considered when the patient's family has a history of unexplained cardiomyopathy or amyloidosis or there's low voltage on EKG or LVH by echo, especially in the patient who is not hypertensive and heavy proteinuria. We should also evaluate for sleep apnea. This is a brief, very simple algorithm for diagnostic steps in patient with suspected heart failure. Again, of course, it starts with the clinical assessment, laboratory studies, diagnostic studies, and then that helps us to determine does that patient have heart failure or not and also helps us to determine the cause and classification. The reason that that is so important is because that then affects our treatment. There are key prognostic parameters to look for to indicate that your patient needs more, perhaps more evaluation or further management or even advanced heart failure modalities. If the patient is having a decreasing left ventricular injection fraction, if their NYHA functional class is worsening, the degree of hyponatremia is important because, again, that indicates severe heart failure. Decreasing peak exercise oxygen uptake, decreasing hematocrit, and a widened QRS on EKG. If the patient is chronically hypotensive, if they have a resting tachycardia or renal insufficiency, if they're intolerant to conventional therapies or they have a refractory volume overload. Again, these are very key prognostic parameters. Our approach to heart failure is comprehensive. We start with the inpatient referral, but we also initially assess patients that are referred as outpatients. With an inpatient referral, the initial consult is placed during the hospitalization. The patient is generally admitted to the hospitalist. They will then typically consult cardiology, who then places a consult for our heart failure team. We have a heart failure coordinator who is an RN educator, and she sees the patient during the admission. She provides general heart failure education with materials, and then she follows that patient, as indicated, during the admission with ongoing education, as indicated, answers questions, and just follows them throughout their hospitalization. She also schedules that patient for a new outpatient heart failure clinic appointment, and we try to get these folks in for their initial visit within one or two weeks of discharge. We also have patients who are referred as an outpatient, and that initial visit is made as a new heart failure clinic appointment. So what happens with that initial heart failure visit as an outpatient? Well, we look at the assessment of history, any testing that's been done to this point. We also proceed with any further testing that may be indicated. There may be a reason during the admission that the patient was unable to have certain testing done, and perhaps needed to wait until their symptoms stabilized. So if there are still additional testing to be done, then we proceed with that. We also further educate that patient, as well as their family. We review the disease process, the treatment plan, the goals for that patient, and the expectations. Expectations that we have of them, as well as that they may have of us. The patient is given a direct contact information into our heart failure staff, and this is very reassuring for a lot of patients. They don't feel that they're out there on their own, and particularly the family members. If the patient is having a specific deterioration in symptoms, they call us. We encourage them to call us, or if there's a question about their treatment, then again, we encourage them to call. We also discuss non-pharmacologic interventions. One of those is vaccinations. We recommend vaccinations against respiratory illnesses. The influenza vaccination has been associated with significant reduction in all-cause mortality, cardiovascular mortality, and cardiovascular hospitalizations. We know that patients with heart failure are at risk of poor outcomes if they develop COVID infection, and they should be vaccinated. We also discuss dietary sodium restriction. The AHA recommends a reduction of sodium intake to less than 2,300 milligrams per day to promote general cardiovascular health, and in patients with heart failure, 2,000 to 3,000 milligrams per day sodium restriction has been shown to improve NYHA functional class and legedema in patients with hep ref. Exercise is also important. We like for our folks to be active. We encourage that, and so we discuss physical activity and cardiac rehab, and this is particularly helpful for family members. A lot of times the patient will come in and say, please tell her that I can do this or that, because the family member is very concerned about the patient. They do not want them to partake in activities that can make them worse, so we discuss that. We know that exercise training is associated with an improvement in functional capacity, in exercise duration, in health-related quality of life, and in the reduction of heart failure hospitalizations in hep ref and hep pef, and cardiac rehab improves functional capacity, exercise duration, and health-related quality of life, so it's important for the patient to be active. The one qualifier I tell the patient is they really need to listen to their body, because as we are seeing these patients, particularly in the early weeks following discharge from the hospital or an initial diagnosis of heart failure, we're going to be making quite a few medication changes, and many of those medications that we will be adjusting lower blood pressure as well as heart rate, and they can affect volume status, so we don't want the patient to become significantly lightheaded more than just when they stand up, because we do not want them to fall or injure themselves, and they really need to be in tune to their body. We want them to go for a walk if they feel like going for a walk, but if they're tired and fatigued and feel like they need to stop and rest, then that's what they need to do. We see our patients for outpatient visits and heart failure every two to three weeks, or as indicated, because we want to very aggressively titrate their medications and manage their symptoms. Some patients may tolerate a much more rapid titration, while others, for various reasons, hypotension, their hemodynamics will just not allow a rapid titration, so we typically see them every two to three weeks. We obtain labs, EKGs, or any other studies that are indicated during the course of these evaluations. We review and follow up on their labs and their diagnostic data, and again, it's very important to follow up with patients on results. If it's important enough to do a lab test, then we need to let the patient know how that looks, good, bad, or if any changes need to be made based on the results. We also evaluate that patient's adherence to both pharmacologic as well as non-pharmacologic management. Our goal, again, is aggressive titration of guideline-directed medical therapies and management of symptoms, and again, we will be discussing in great detail the guideline-directed therapies in a later module. Once the patient is on a targeted dose of their guideline-directed therapy or on the maximum tolerated dosage for that patient, then we reassess their ejection fraction. At this point, we need to determine if that patient needs to be considered for device implants. Will they need a prophylactic ICD or cardiac resynchronization therapy? And if the ejection fraction remains 35% or lower, we make a referral as indicated to our electrophysiologist. Once that patient is stable on guideline-directed therapies or the maximum tolerated dosage for them, then the visits become more spread out. We typically see them every three to six months, but that may vary according to their condition. Of course, they always have the direct phone line into our heart failure staff, so if something changes from their perspective, they know they can call us. We also try to coordinate any visits to our heart failure clinic with their primary cardiology follow-up so that we can avoid overlap. Our goal is to achieve optimal guideline-directed medical therapy within three to six months of the initial diagnosis of heart failure. So the next few slides are just references that were referred to during the presentation. In our next module, we will be discussing extensively guideline-directed medical therapies for patients with heart failure. So thank you for joining us for the introduction to heart failure. We hope to see you in the next module.

heart failure

introduction

Sandy McCrary

diagnostic tools

risk factors

management

guidelines