Does Heart Failure With Preserved Ejection Fraction Have an Overused Label?

A Critical Exploration of HFpEF’s Expanding Diagnosis, Its Ambiguities, and Its Clinical Consequences

In the evolving field of cardiology, Heart Failure with Preserved Ejection Fraction (HFpEF) has become a common and, some argue, overly generous diagnosis. It now accounts for more than 50% of heart failure cases, particularly among older adults, women, and patients burdened with multiple comorbidities. However, as clinical experience with the label grows, so does skepticism. Many cardiologists and internists are beginning to ask: Are we overusing this term?

Unlike Heart Failure with Reduced Ejection Fraction (HFrEF), which has a relatively well-defined pathophysiology and robust treatment framework, HFpEF remains shrouded in diagnostic ambiguity. The combination of nonspecific symptoms, limited therapeutic options, and unclear underlying mechanisms often turns this diagnosis into a repository for diagnostic uncertainty—especially when echocardiograms are "normal."

This article critically examines whether HFpEF is being used too liberally, misunderstood, or misapplied—and explores its consequences for patients, clinicians, and the broader field of cardiology.

Understanding the Definition of HFpEF

Traditionally, HFpEF has been defined as heart failure in patients who:

• Exhibit signs and symptoms of heart failure
  
  
• Demonstrate a left ventricular ejection fraction (LVEF) of ≥50%
  
  
• Have additional evidence of diastolic dysfunction, elevated natriuretic peptides, or structural heart disease (such as left atrial enlargement or left ventricular hypertrophy)
  

However, LVEF alone is insufficient to capture the complex physiologic nuances at play. It fails to reflect elevated left ventricular filling pressures, reduced myocardial compliance, and diminished cardiac reserve under physical stress.

In many instances, the HFpEF label may actually be masking conditions such as:

• Age-related vascular stiffening
  
  
• Obesity-related ventilatory restriction
  
  
• Atrial fibrillation and associated hemodynamic effects
  
  
• Chronic pulmonary disease
  
  
• Anemia or poor physiologic reserve
  

In such scenarios, HFpEF becomes more a diagnosis of default than of precision.

The Diagnostic Dilemma: Are We Too Quick to Use the Term?

In day-to-day clinical practice—especially in time-constrained hospital wards and outpatient clinics—the equation of “shortness of breath + normal EF = HFpEF” has become a dangerously convenient heuristic.

This has led to a phenomenon of diagnostic inflation, where:

• Patients are labeled with HFpEF without comprehensive assessment of diastolic function
  
  
• Natriuretic peptides such as BNP or NT-proBNP are interpreted without accounting for confounding variables like obesity
  
  
• Other potential causes of dyspnea, particularly in older adults, are insufficiently explored
  

The risk here is not merely academic. Overdiagnosing HFpEF leads to misdirected treatment strategies and delays in addressing more reversible conditions like chronic lung disease, iron deficiency, or even poor cardiovascular conditioning.

Clinical Heterogeneity of HFpEF: A Spectrum or a Syndrome?

One of the most challenging aspects of HFpEF is its broad and variable presentation. It is not a single disease but rather a clinical syndrome encompassing a variety of overlapping phenotypes:

• Metabolic phenotype: Often seen in obese and diabetic patients, typically featuring insulin resistance, concentric LV hypertrophy, and systemic inflammation
  
  
• Hypertensive phenotype: Marked by long-standing hypertension and diastolic stiffening
  
  
• Atrial fibrillation phenotype: Where rhythm abnormalities precede and complicate cardiac performance
  
  
• Pulmonary vascular phenotype: Coexistent COPD or pulmonary hypertension creating a shared burden of dyspnea
  

The crucial clinical implication is this: when we diagnose HFpEF, what are we really treating? The heart? The lungs? The metabolic syndrome? This lack of specificity can lead to scattershot management and therapeutic uncertainty.

Does Overuse Dilute the Term’s Clinical Meaning?

The growing prevalence of the HFpEF label has potential consequences:

• It encourages diagnostic complacency, with clinicians halting further workup once HFpEF is suggested
  
  
• It promotes therapeutic nihilism, given the limited treatment options and lack of consensus on best practices
  
  
• It may generate patient distress, as the phrase "heart failure" carries weight, stigma, and implications for employment, insurance, and mental health
  
  
• It can weaken clinical research, as overly inclusive diagnostic criteria lead to heterogeneous study populations and inconclusive trial results
  

In short, when used indiscriminately, the HFpEF label can do more harm than good.

The Pathophysiological Complexity: We Don’t Fully Understand HFpEF

While the pathophysiology of HFrEF centers on impaired systolic function, HFpEF remains elusive. Multiple interrelated mechanisms have been proposed:

• Impaired diastolic relaxation and increased ventricular stiffness
  
  
• Systemic and endothelial inflammation
  
  
• Microvascular dysfunction
  
  
• Altered skeletal muscle metabolism
  
  
• Autonomic imbalance and chronotropic incompetence
  

The growing consensus is that HFpEF represents a multisystem disorder, not just a cardiac anomaly. This shift in understanding makes precise diagnosis more important—and more difficult.

Are Current Diagnostic Tools Adequate?

The answer, unfortunately, is often no. Resting transthoracic echocardiograms, while standard, are usually normal in patients with HFpEF, especially at rest. Advanced diagnostic tools include:

• Diastolic stress echocardiography, which evaluates filling pressures during exercise
  
  
• Invasive hemodynamic studies, measuring pulmonary capillary wedge pressure under load
  
  
• The H2FPEF score, a structured algorithm that incorporates clinical and imaging data (e.g., BMI, age, atrial fibrillation, BNP)
  

Despite their promise, these tools are rarely employed outside of academic or specialized settings. Most clinicians continue to default to symptoms plus a preserved LVEF—a practice that, while understandable, risks underdiagnosis or overdiagnosis depending on the context.

Therapeutic Limitations: Are We Treating Anything Differently?

Until recently, treatment options for HFpEF were limited. The primary approach has been symptom relief and comorbidity management:

• Diuretics for volume control
  
  
• Antihypertensives for blood pressure regulation
  
  
• Lifestyle interventions (weight loss, exercise, sodium restriction)
  
  
• Rhythm control or rate control in atrial fibrillation
  

However, the therapeutic landscape is evolving:

• SGLT2 inhibitors, such as empagliflozin, have demonstrated benefits in HFpEF patients regardless of diabetic status
  
  
• Mineralocorticoid receptor antagonists, like spironolactone, show selective benefit in specific subgroups
  
  
• ARNIs (angiotensin receptor–neprilysin inhibitors), such as sacubitril/valsartan, offer mild improvements, though results vary depending on ejection fraction range
  

Nevertheless, the majority of treatment remains empiric, and simply applying the HFpEF label does not guarantee a pathway to targeted therapy. Many patients are still left in a therapeutic limbo.

Why the Label Still Has Value—When Used Correctly

Despite the criticisms, HFpEF is not a useless diagnosis. When made carefully, it provides meaningful clinical value:

• Risk stratification: Patients with HFpEF face high morbidity and mortality risks
  
  
• Standardization: It offers a common language for physicians across specialties
  
  
• Research opportunities: The label helps identify suitable trial populations and focus future therapeutic innovation
  
  
• Patient motivation: A heart failure diagnosis, framed correctly, can encourage adherence to lifestyle changes and comorbidity management
  

However, its value hinges on diagnostic accuracy and contextual application. Misuse diminishes its utility; judicious application preserves its relevance.

How to Avoid Overdiagnosis of HFpEF

To improve diagnostic fidelity, physicians should:

• Thoroughly rule out non-cardiac causes of dyspnea, including deconditioning, COPD, anemia, and obesity
  
  
• Interpret natriuretic peptide levels in clinical context, especially considering that obese patients may have falsely low values
  
  
• Use echocardiography not just to assess LVEF, but to examine diastolic function, left atrial size, and pulmonary pressures
  
  
• Apply validated tools such as the H2FPEF score when the diagnosis is uncertain
  
  
• Recognize that HFpEF is a diagnosis of exclusion, not a shortcut when the cause of symptoms is unclear
  

By approaching the diagnosis methodically, clinicians can reduce overlabeling and avoid the pitfalls of premature closure.

Conclusion: Be Careful with the Label

HFpEF is real—but so is the risk of overdiagnosis.

Too often, the term is applied without a thorough workup or a critical consideration of alternative explanations. While the diagnosis can guide management and prognosis, its overuse can lead to therapeutic inertia, diagnostic confusion, and patient anxiety.

Instead of applying the label as a default, clinicians should reserve it for cases where structured evaluation supports the diagnosis and therapeutic decisions can meaningfully follow. Labels in medicine are powerful. They can clarify, but they can also mislead. HFpEF deserves careful, deliberate use—not casual assignment.