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Heart failure with preserved ejection fraction: Clinical manifestations and diagnosis

Heart failure with preserved ejection fraction: Clinical manifestations and diagnosis
Literature review current through: Jan 2024.
This topic last updated: Jul 25, 2023.

INTRODUCTION — Heart failure with preserved ejection fraction (HFpEF) is a clinical syndrome in patients with current or prior symptoms of HF with a left ventricular ejection fraction (LVEF) ≥50 percent and evidence of cardiac dysfunction as the cause of symptoms (eg, abnormal LV filling pattern and elevated filling pressures) [1-5]. Previously, HFpEF was termed "diastolic HF."

The clinical manifestations and diagnosis of patients with HFpEF will be reviewed here.

Issues related to pathophysiology, epidemiology, treatment, and prognosis are discussed separately.

(See "Pathophysiology of heart failure with preserved ejection fraction".)

(See "Epidemiology of heart failure".)

(See "Treatment and prognosis of heart failure with preserved ejection fraction".)

(Related Pathway(s): Heart failure: Diagnosis and classification.)

Asymptomatic LV diastolic dysfunction is discussed separately. (See "Asymptomatic left ventricular diastolic dysfunction".)

CLINICAL MANIFESTATIONS

The clinical manifestations of HFpEF are generally the same as those for other forms of HF (eg, HF with reduced ejection fraction [HFrEF]) [6-8]. Dyspnea (including dyspnea on exertion, paroxysmal nocturnal dyspnea, and orthopnea) and fatigue are the most common symptoms of HFpEF (table 1) [9]. Exertional chest pain is also a common presentation in patients with HFpEF [10]. (See "Heart failure: Clinical manifestations and diagnosis in adults", section on 'Clinical presentation'.)

In general, signs and symptoms alone cannot be used to differentiate HFpEF from HFrEF:

In a report in which the clinical data from 59 patients aged at least 60 years old with symptoms of HF and an LVEF ≥50 percent were compared with data from 60 patients of the same age with HF and an LVEF ≤35 percent and with data from 28 age-matched healthy controls, the patients with HFpEF had similar clinical manifestations (including peak oxygen consumption [VO2] and neurohumoral activation) to those with HFrEF, although some parameters were less severe (natriuretic peptide levels, some quality-of-life measures) [11].

In other series, cardiopulmonary exercise parameters, central cardiac filling pressures, and pulmonary hypertension severity were indistinguishable between patients with HFpEF and HFrEF [12,13].

EVALUATION

When to suspect HFpEF — We suspect HFpEF if the history or physical examination reveal at least one symptom (table 1) of HF that is not sufficiently explained by another diagnosis. In patients with symptoms of HF, the presence of certain conditions increases the likelihood that HFpEF is present:

Age ≥60 years

Obesity

Hypertension

Coronary artery disease

Atrial fibrillation (AF)

Diabetes

Chronic kidney disease

In the presence of a noncardiac disease that causes HF-like symptoms or a cardiac disease that causes HF, we consider the following prior to evaluation:

Presence of a noncardiac disease that mimics HF In patients with a history of a noncardiac disease (eg, obesity, chronic kidney disease) that may cause one or more of the signs or symptoms of HF, HFpEF may contribute to the overall burden of symptoms. In such cases, the decision to pursue the diagnosis of HFpEF depends on the likelihood that treatment of HFpEF would improve the patient's symptoms, reduce the risk of adverse events attributable to HFpEF (eg, hospitalization), alter management of preexisting disease, or inform prognosis. (See 'Noncardiac conditions' below.)

Presence of another cardiac disease – In the presence of a cardiac disease known to cause the clinical syndrome of HF or that is associated with the presence of diastolic dysfunction, we typically do not pursue the diagnosis of HFpEF. Such diseases include:

Cardiomyopathy (eg, hypertrophic or restrictive cardiomyopathy)

Cardiac amyloidosis

Significant valve disease (moderate or severe stenosis or regurgitation)

Pericardial disease (eg, constrictive pericarditis)

High-output HF

Diagnostic evaluation — In patients with suspected HFpEF, we suggest the following approach to evaluation (algorithm 1):

Initial testing — The initial evaluation of patients with suspected HFpEF commonly includes the following tests:

Chest radiograph – A chest radiograph is commonly obtained in patients with HF to assess for signs of pulmonary edema and identify other causes of dyspnea. The chest radiograph may show cardiomegaly with or without evidence of pulmonary edema. Most patients with HFpEF have a normal chest radiograph [14]. Thus, normal chest radiography does not exclude HFpEF.

ECG – An electrocardiogram (ECG) is routinely performed in patients with HF, although the findings are often nonspecific. Evidence of myocardial ischemia or prior infarction may be present. AF is observed in approximately 40 to 50 percent of patients with HFpEF, and the lifetime risk of AF in patients with HFpEF is approximately 67 percent [15]. The presence of AF on ECG in a patient with normal LVEF and dyspnea increases the odds that HFpEF is present by more than 20-fold [16].

Echocardiography – If echocardiography has not been performed, we obtain a complete Doppler echocardiogram. Echocardiography can identify abnormal diastolic function and other causes of HF (eg, pericardial disease, valve disease), and is required to calculate the H2FPEF score. (See 'Assessment after initial testing' below.)

Key measures obtained by echocardiography include:

Left ventricular ejection fraction – The presence of an LVEF ≥50 percent is required for the diagnosis of HFpEF. (See "Tests to evaluate left ventricular systolic function", section on 'Echocardiography'.)

Pulmonary artery systolic pressure – Elevation in pulmonary artery systolic pressure (PASP) estimated by echocardiography is common in patients with HFpEF, and the identification of an elevated PASP in an older patient with dyspnea raises suspicion for the diagnosis of HFpEF [17]. PASP >35 mmHg is a criterion of HFpEF diagnostic scores.

Methodology for estimating PASP and limitations of such estimates are discussed separately. (See "Echocardiographic assessment of the right heart", section on 'Pulmonary artery pressure'.)

Signs of abnormal diastolic function and elevated filling pressures – Echocardiography can be used to measure functional parameters suggestive of diastolic dysfunction (eg, E/e’ ratio) that support the diagnosis of HFpEF. The approach to echocardiographic assessment of diastolic dysfunction is discussed separately. (See "Echocardiographic evaluation of left ventricular diastolic function in adults".)

The findings of left atrial enlargement or concentric LV remodeling or hypertrophy can support the diagnosis of HFpEF or lead the clinician to suspect HFpEF but are not necessary to reach the formal diagnosis of HFpEF.

If structural parameters cannot be adequately measured by echocardiography, we suggest obtaining cardiovascular magnetic resonance imaging, although slight differences in measures among imaging modalities have been reported [18].

Natriuretic peptides – We do not typically obtain a natriuretic peptide level as a component of the initial evaluation, but some experts do obtain either a B-type natriuretic peptide (BNP) or N-terminal pro-BNP (NT-proBNP) level as part of initial testing. The use of BNP in the diagnosis of HFpEF is discussed elsewhere in this topic. (See 'Approach to additional testing' below.)

Assessment after initial testing — After initial testing, we evaluate whether the following are present (algorithm 1):

At least one symptom or sign of HF

Evidence of an LVEF ≥50 percent

No apparent cause of HF symptoms other than HFpEF

In patients without one or more of these factors, isolated HFpEF is unlikely to be present. However, some patients may nonetheless have HFpEF caused by another cardiac disease, such as valve disease, pulmonary arterial hypertension, or pericardial disease. In such cases, we suggest referral to a general cardiologist or HF cardiologist to determine whether HFpEF is present and the best approach to treatment.

In patients in whom all three factors are present, we calculate the likelihood that HFpEF is present. We prefer to use the "Heavy, Hypertensive, atrial Fibrillation, Pulmonary hypertension, Elder, and Filling pressure" (H2FPEF) score (calculator 1), which estimates the likelihood that symptoms are best explained by HFpEF. The score is the sum of points assigned to the following clinical variables (scores range 0 to 9) (algorithm 1) [14]:

Heavy – Body mass index >30 kg/m2 (2 points) (calculator 2).

Hypertensive – Hypertensive and treated with two or more antihypertensive medicines (1 point).

Atrial Fibrillation – Any history of paroxysmal or persistent AF (3 points).

Pulmonary hypertension – PASP >35 mmHg using Doppler echocardiography (1 point).

Elder – Age >60 years (1 point).

Filling pressure – Doppler echocardiographic E/e' >9 (1 point) where E is the peak velocity of early LV filling and e' is the peak early diastolic velocity of LV myocardium adjacent to the mitral annulus by tissue Doppler.

The likelihood that HFpEF is present depends on the H2FPEF score value (algorithm 1):

0 points – In patients with a H2FPEF score of 0, the likelihood that HFpEF is the cause of symptoms is low (ie, 14 percent); in such cases, we typically search for other causes of the patient’s symptoms.

1 to 5 points – In patients with 1, 2, 3, 4, or 5 points, the likelihood that HFpEF is the cause of symptoms is low or intermediate (ie, 24, 40, 56, 72, and 84 percent); in such cases, additional testing is required. (See 'Approach to additional testing' below.)

6 or more points – In patients with 6, 7, 8, or 9 points, HFpEF is the most likely the cause of symptoms (ie, 91, 95, 98, and 99 percent), and no further testing for the cause of symptoms is required.

The American guidelines mention the use of diagnostic scores and state no preference for use of a specific score [19]. The European Society of Cardiology favors use of the "Heart Failure Association Pretest assessment, Echocardiography and natriuretic peptide, Functional testing, Final etiology" (HFA-PEFF) [18].

Our preference to use a score to diagnose HFpEF is based on the syndromic nature of HFpEF. In our experience and based on limited data, other approaches to diagnosis (eg, single criterion from echocardiography, natriuretic peptide levels) are less accurate for the diagnosis of HFpEF. The H2FPEF score has greater accuracy than the HFA-PEFF score and was validated using the gold standard of exercise hemodynamic measurements [20]:

In a study that included patients who underwent a hemodynamic exercise test, the H2FPEF score had a higher diagnostic accuracy than the HFA-PEFF score (area under the receiver operator curve 0.85 versus 0.71; difference 0.13, 95% CI 0.1-0.18) [21]. The accuracy of the H2FPEF score was higher in all subgroups tested (eg, patients with or without obesity, AF, elevated BNP levels, chronic kidney disease).

The H2FPEF score was derived based on data from 414 patients with an LVEF ≥50 percent (267 with HFpEF and 147 with noncardiac dyspnea) and validated in a test cohort of 100 patients (61 with HFpEF) [14]. Diagnoses for all patients were validated by an invasive hemodynamic exercise test. The odds of HFpEF doubled for each one-unit increase in the H2FPEF score (odds ratio 1.98, 95% CI 1.74-2.30), and area under the curve was 0.84. The H2FPEF score was more accurate than an algorithm based on expert consensus (increase in area under the curve of 0.17, 95% CI 0.12-0.22). Inclusion of natriuretic peptide levels did not improve the accuracy of the model.

Approach to additional testing — In patients in whom there remains a clinical suspicion for HFpEF but in whom the H2FPEF score does not suggest the presence of HFpEF (ie, score between 1 and 5), we perform additional testing (algorithm 1):

First, natriuretic peptide testing – In patients in whom there is diagnostic uncertainty after initial testing, the next step in evaluation is to obtain a serum natriuretic peptide level (ie, BNP or NT-proBNP). However, in patients with chronic kidney disease and markedly reduced estimated glomerular filtration rate (eGFR; eg, <30 mL/min/1.73 m2) or other conditions (eg, obesity (table 2)) in which the natriuretic peptide levels are unlikely to accurately represent filling pressures, we suggest referral to a general cardiologist or HF cardiologist to guide further testing. (See "Natriuretic peptide measurement in heart failure", section on 'Impact of conditions and medications'.)

In patients in whom natriuretic peptide levels are unlikely to be markedly influenced by other conditions, the interpretation of the BNP levels for the diagnosis of HFpEF is as follows:

If the NT-proBNP level is >450 pg/mL or BNP is >150 pg/mL, the presence of HFpEF is highly likely, and no further testing is necessary.

If the NT-proBNP level is ≤450 pg/mL or BNP is ≤150 pg/mL, the diagnosis of HFpEF is not excluded; there is no rule-out value for NT-proBNP or BNP. In such patients, additional testing is required (algorithm 1).

If the diagnosis of HFpEF is not confirmed after BNP testing (eg, natriuretic peptide level not representative of filling pressures, high clinical suspicion), the next step in the diagnostic evaluation is measurement of invasive hemodynamics (see below).

Our approach to the use of natriuretic peptides differs from North American and European guidelines, which are unclear on the exact role of natriuretic peptides in the diagnosis of HFpEF [19,22].

This approach is based on our experience and limited data that studied different thresholds for BNP levels:

In one study, an NT-proBNP level >450 pg/mL was 85 percent specific for HFpEF [16].

A large series of consecutive patients showed that 60 percent of patients with invasively proven HFpEF had NT-proBNP levels <260 pg/mL, and 37 percent had NT-proBNP levels <125 pg/mL [23].

Further details on BNP testing can be found separately. (See "Natriuretic peptide measurement in heart failure".)

If uncertainty remains, obtain invasive hemodynamic measurements – In patients in whom HFpEF is suspected but cannot be confirmed or excluded by other means, we obtain a right heart catheterization and, if indicated, hemodynamics measured during maneuvers that increase LV filling pressures. Prior to invasive testing, we suggest cardiology consultation to review all available data, review the risks and benefits of invasive testing, and assist with interpretation of right heart catheterization findings [3,24-26].

Invasive testing protocol – The elements of a hemodynamic for assessment of HFpEF include:

-Pressures should be measured at end-expiration with an open glottis.

-If pulmonary capillary wedge pressure (PCWP) is not ≥15 mmHg at rest, we perform invasive measurements with maneuvers to increase LV filling pressures. We typically use supine cycle ergometry (60 rotations per minute beginning at 20 W and increasing by 10 to 20 W increments every two to three minutes until exhaustion) [16,24]. We prefer exercise hemodynamics rather than fluid boluses, leg raises, or other maneuvers designed to load the LV; in patients with HFpEF, exercise causes more pronounced elevations in filling pressures than other maneuvers [26].

-If exercise is not possible, a passive leg raise can be used.

Invasive test interpretation – The interpretation of hemodynamics and the need for exercise testing are as follows:

-Resting measurements – In patients with PCWP ≥15 mmHg at rest, the presence of HFpEF is confirmed. In patients with normal resting filling pressures, the diagnosis of HFpEF is not excluded [27].

-Exercise measurements – In patients with an increase in PCWP to ≥25 mmHg at any point during a supine exercise effort or maneuver designed to increase LV filling pressures, the presence of HFpEF is confirmed.

In patients undergoing upright exercise, if the increase in PCWP relative to the increase in cardiac output exceeds 2 mmHg/L/min, the presence of HFpEF is confirmed [28].

In patients without an elevated PCWP with exercise, the diagnosis of HFpEF is excluded.

Right heart catheterization with exercise is recognized as the clinical gold standard for the diagnosis of HFpEF by professional societies [19,22]. However, these societies also recognize the use of a diastolic stress test as a noninvasive option that can be used to diagnose HFpEF. In our experience, diastolic stress tests are difficult to conduct, are not widely available, and have lower accuracy than invasive hemodynamic testing. (See 'Tests with limited value' below.)

In addition, approximately 35 percent of patients with HF have normal PCWP at rest and only exhibit abnormal hemodynamics with exercise [27].

Tests with limited value — Tests with an unclear role in the diagnosis of HFpEF include:

Cardiopulmonary exercise test – Noninvasive cardiopulmonary exercise testing has a limited role in differentiating patients with HF from those with lung disease and deconditioning [12]:

In a large study with invasive evaluation for HFpEF, cardiopulmonary exercise testing had low sensitivity and specificity for HFpEF and noncardiac causes of dyspnea [29].

In a large study, a peak oxygen consumption (VO2) of less than 14 mL/min/kg was highly specific for HFpEF, and patients with values higher than 20 mL/min/kg were unlikely to have HFpEF. However, peak VO2 between 14 to 20 mL/min/kg neither confirmed nor excluded the presence of HFpEF. (See "Approach to the patient with dyspnea", section on 'Cardiopulmonary exercise testing'.)

Exercise echocardiography – Some studies suggest that there may also be a role for exercise echocardiography in the evaluation of HFpEF, but there are conflicting data on its accuracy [25,30-32]. (See "Echocardiographic evaluation of left ventricular diastolic function in adults", section on 'Tissue Doppler imaging'.)

DIFFERENTIAL DIAGNOSIS

Noncardiac conditions — Among patients who have an LVEF ≥50 percent and symptoms or signs suggestive of HF (such as shortness of breath, ankle edema, or paroxysmal nocturnal dyspnea), some do not have HF but have one or more other conditions such as obesity, deconditioning, advanced age, venous insufficiency, anemia, or lung disease.

Cardiac conditions — Cardiac diseases that may present with HF (table 3) or that may be complicated by diastolic dysfunction or HFpEF but that require a different approach to management include the following conditions:

Coronary artery disease – Obstructive coronary artery disease (CAD) can cause exertional dyspnea that can mimic the symptoms of HFpEF. Obstructive CAD may also cause HFpEF. The approach to CAD assessment is described elsewhere in this topic. (See 'Testing for coronary artery disease' below.)

Restrictive cardiomyopathy – Restrictive cardiomyopathy is characterized by nondilated ventricles with severely impaired ventricular filling, which is caused by a variety of familial and nonfamilial conditions. The characteristics of restrictive cardiomyopathy that differentiate it from HFpEF are described separately. (See "Restrictive cardiomyopathies", section on 'When to suspect RCM'.)

In patients diagnosed with HFpEF, cardiac amyloidosis may be present. If there are other signs or symptoms of amyloidosis, further testing for amyloid is required [33]. In addition, a clinical score may be used to identify patients at particularly high risk of cardiac amyloidosis [34]. The signs and symptoms of amyloidosis and the approach to its diagnosis are discussed separately. (See "Cardiac amyloidosis: Epidemiology, clinical manifestations, and diagnosis".)

Hypertrophic cardiomyopathy – Hypertrophic cardiomyopathy (HCM) is commonly caused by a mutation in one of several sarcomeric genes and is differentiated from HFpEF by characteristic clinical features and echocardiographic findings. (See "Hypertrophic cardiomyopathy: Clinical manifestations, diagnosis, and evaluation".)

In addition to sarcomeric (ie, genetic) HCM, other causes of HCM include glycogen storage disease, lysosomal disease (including Fabry disease), syndromic HCM (eg, Noonan syndrome, LEOPARD syndrome [lentigines, ECG abnormalities, ocular hypertelorism, pulmonic stenosis, abnormal genitalia, retardation of growth, and sensorineural deafness], Friedreich ataxia), and familial amyloidosis (transthyretin [TTR] or apolipoprotein mutation). (See "Noonan syndrome" and "Congenital and inherited hyperpigmentation disorders", section on 'LEOPARD syndrome' and "Friedreich ataxia" and "Inherited syndromes associated with cardiac disease", section on 'Metabolic disorders'.)

Noncompaction – LV noncompaction (LVNC) is a cardiomyopathy characterized by prominent LV trabeculae and deep intertrabecular recesses, resulting in a thickened myocardium consisting of a noncompacted layer and a thin compacted layer. Although LVNC was traditionally considered a developmental anomaly, acquired cases have been reported. Although many patients with HF and LVNC have a reduced LVEF, some have an LVEF ≥50 percent. (See "Isolated left ventricular noncompaction in adults: Clinical manifestations and diagnosis".)

Valve disease – This is generally differentiated from HFpEF by echocardiography showing abnormal valve function. Of note, many patients with HFpEF also display some evidence of valvular heart disease, but not in the severe range. Mild to moderate valve lesions in patients with HFpEF are generally considered to be "bystanders" rather than causal of HF symptoms; nonsevere mitral and tricuspid regurgitation are common in HFpEF. The presence of mild to moderate mitral regurgitation in HFpEF is an indicator of more severe left atrial myopathy and is also related to the presence of atrial fibrillation [35]. Tricuspid regurgitation is also commonly associated with AF and also suggests the presence of right HF [36].

Pericardial disease – Pericardial disease, such as constrictive pericarditis, can be differentiated from isolated HFpEF with echocardiography or other tests. (See "Constrictive pericarditis: Diagnostic evaluation".)

High-output heart failure – High-output HF may present similarly to HFpEF and has many of the same features. The presence of an elevated cardiac index and chamber enlargement at rest suggest the presence of a high-output state. (See "Clinical manifestations, diagnosis, and management of high-output heart failure", section on 'When to suspect high-output heart failure'.)

Obstructive heart disease – An obstructive lesion in great vessel or heart, such as an intracardiac mass or pulmonary vein stenosis can mimic HFpEF. Cardiac masses are typically evident on echocardiography, while pulmonary vein stenosis is suggested by symptoms and an appropriate history (eg, history of catheter ablation near or within pulmonary veins). The evaluation for these conditions is described elsewhere. (See "Cardiac tumors" and "Atrial fibrillation: Catheter ablation", section on 'Pulmonary vein stenosis'.)

Right-sided heart failure – Right HF due to non-HFpEF causes (including right ventricular [RV] infarction, arrhythmogenic RV cardiomyopathy, and pulmonary arterial hypertension not due to left heart disease) may present similarly to HFpEF. These diagnoses are usually suggested by echocardiography. (See "Right ventricular myocardial infarction" and "Arrhythmogenic right ventricular cardiomyopathy: Anatomy, histology, and clinical manifestations" and "Clinical features and diagnosis of pulmonary hypertension of unclear etiology in adults".)

However, many patients with HFpEF display concurrent RV dysfunction, tricuspid insufficiency, and right HF, or go on to develop right HF that may be difficult to distinguish from the above causes of right HF when followed longitudinally [37-39]. The development of right HF is associated with worse outcomes. A majority of patients with HFpEF (>80 percent) also display pulmonary hypertension (PH) secondary to chronic elevation in left heart pressures, and RV dysfunction associated with PH is also common [17,37,38]. It is important to distinguish PH caused by HFpEF from other types of PH. (See "Pulmonary hypertension due to left heart disease (group 2 pulmonary hypertension) in adults" and "Clinical features and diagnosis of pulmonary hypertension of unclear etiology in adults".)

TESTING FOR CORONARY ARTERY DISEASE — CAD is common in patients HFpEF, seen in approximately two-thirds of patients in angiographic and autopsy studies, and is a potentially reversible cause of HFpEF [40-42]. We evaluate for CAD in the following scenarios:

Symptoms suggestive of obstructive CAD – In patients with HFpEF who have symptoms that suggest the presence of obstructive CAD (eg, angina, dyspnea on exertion), which may be anginal equivalents, or who have signs of myocardial infarction or ischemia on imaging, we suggest an evaluation for CAD.

New diagnosis of HFpEF and known CAD – In patients who present with HFpEF and known CAD without angina, we evaluate for the presence of ischemia unless the patient is not eligible for revascularization [43]. (See "Stress testing for the diagnosis of obstructive coronary heart disease" and "Selecting the optimal cardiac stress test".)

Asymptomatic patients without history of CAD – In patients with HFpEF and no history of CAD, we do not routinely test for obstructive CAD.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Heart failure in adults".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topic (see "Patient education: Heart failure with preserved ejection fraction (The Basics)")

Beyond the Basics topic (see "Patient education: Heart failure (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

Clinical manifestations – The clinical manifestations of HFpEF are generally the same as those for other forms of HF (eg, HF with reduced ejection fraction [HFrEF]) (table 1). Exertional chest pain is also a common presentation in patients with HFpEF.

When to suspect HF – We suspect HFpEF if the history or physical examination reveal at least one symptom (table 1) of HF that is not sufficiently explained by another diagnosis. In patients with symptoms of HF, the presence of certain factors (eg, age >60 years, hypertension, diabetes) increases the likelihood of HFpEF (algorithm 1). (See 'When to suspect HFpEF' above.)

Initial testing – The initial testing for HFpEF includes a chest radiograph, ECG, and echocardiography. (See 'Initial testing' above.)

Assessment after initial testing – After initial testing, we evaluate whether the following are present (algorithm 1) (see 'Assessment after initial testing' above):

At least one symptom or sign of HF

Evidence of a left ventricular ejection fraction (LVEF) ≥50 percent

No apparent cause of HF symptoms other than HFpEF

In patients without one or more of these factors, HFpEF is unlikely to be present.

In patients in whom all these factors are present, we calculate the likelihood that HFpEF is present. We prefer to use the "Heavy, Hypertensive, atrial Fibrillation, Pulmonary hypertension, Elder, and Filling pressure" (H2FPEF) score (calculator 1), which estimates the likelihood that symptoms are best explained by HFpEF (algorithm 1):

0 points – In patients with a H2FPEF score of 0 points, the likelihood that HFpEF is the cause of symptoms is low; in such cases, we typically search for other causes of the patient's symptoms.

1 to 5 points – In patients with 1, 2, 3, 4, or 5 points, the likelihood that HFpEF is the cause of symptoms is intermediate; in such cases, additional testing is required.

6 or more points – In patients with 6, 7, 8, or 9 points, HFpEF is most likely the cause of symptoms, and no further testing for the cause of symptoms is required.

Approach to additional testing – In patients in whom there remains a clinical suspicion for HFpEF but in whom the H2FPEF score does not suggest the presence of HFpEF (ie, score between 2 and 5, score of 1 and high clinical suspicion), we perform additional testing (algorithm 1):

Natriuretic peptide testing – In patients in whom there is diagnostic uncertainty after initial testing, the next step in evaluation is to obtain a serum natriuretic peptide level (ie, B-type natriuretic peptide [BNP] or N-terminal pro-BNP [NT-proBNP]). However, in patients with chronic kidney disease and markedly reduced estimated glomerular filtration rate (eGFR; eg, <30 mL/min/1.73 m2) or other conditions (eg, obesity (table 2)) in which the natriuretic peptide levels are unlikely to accurately represent filling pressures, we suggest referral to a general cardiologist or HF cardiologist to guide further testing. (See "Natriuretic peptide measurement in heart failure", section on 'Impact of conditions and medications'.)

In patients in whom natriuretic peptide levels are unlikely to be markedly influenced by other conditions, the interpretation of the BNP levels for the diagnosis of HFpEF is as follows:

-If the NT-proBNP level is >450 pg/mL or BNP is >150 pg/mL, the presence of HFpEF is highly likely, and no further testing is necessary.

-If the NT-pro-BNP level is ≤450 pg/mL or BNP is ≤150 pg/mL, the diagnosis of HFpEF is not excluded; NT-proBNP and BNP cannot be used to rule out HFpEF. In such patients, additional testing is required (algorithm 1).

If uncertainty remains, invasive hemodynamic testing – In patients in whom HFpEF is suspected but cannot be confirmed or excluded by other means, we obtain a right heart catheterization and, if indicated, hemodynamics measured during maneuvers that increase LV filling pressures. (See 'Approach to additional testing' above.)

Tests with limited value – Tests with limited value include cardiopulmonary exercise testing and exercise echocardiography. (See 'Tests with limited value' above.)

Differential diagnosis – Among patients who have an LVEF ≥50 percent and symptoms or signs suggestive of HF, some do not have HF but have one or more other conditions such as obesity, deconditioning, advanced age, venous insufficiency, or lung disease. (See 'Noncardiac conditions' above.)

Cardiac diseases that may present with HF (table 3) or that may be complicated by diastolic dysfunction or HFpEF but that require a different approach to management include coronary artery disease (CAD), hypertrophic cardiomyopathy (HCM), and cardiac amyloidosis. (See 'Cardiac conditions' above.)

Testing for coronary artery disease – In patients with suspected HFpEF whose history is not concerning for new or worsening angina, we do not routinely test for the presence of CAD.

ACKNOWLEDGMENTS

The UpToDate editorial staff acknowledges Michael R Zile, MD, who contributed to earlier versions of this topic review.

The UpToDate editorial staff also acknowledges William H Gaasch, MD (deceased), and William C Little, MD (deceased), who contributed to earlier versions of this topic.

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Topic 3504 Version 55.0

References

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