HFpEF (pronounced “hef-pef”) stands for heart failure with preserved ejection fraction. It’s a type of heart failure where the heart pumps out a normal amount of blood with each beat, but the heart muscle has become too stiff to fill properly between beats. The ejection fraction, a measure of how much blood the heart pushes out each time it contracts, remains at 50% or above. That number looks normal on paper, which is part of why this condition was historically overlooked and remains harder to diagnose than other forms of heart failure.
HFpEF now accounts for roughly half of all heart failure cases, and its prevalence is rising as populations age and obesity rates climb. Despite the “preserved” label, the prognosis is serious: five-year mortality is close to 60%, nearly identical to heart failure where the pumping function is clearly reduced.
How HFpEF Differs From Other Heart Failure
Heart failure is classified by ejection fraction into distinct categories. In heart failure with reduced ejection fraction (HFrEF), the heart muscle is weakened and pumps out 40% or less of its blood volume. There’s also a middle category, heart failure with mildly reduced ejection fraction (HFmrEF), covering ejection fractions of 41% to 49%. In HFpEF, the ejection fraction sits at 50% or higher.
The difference matters because the underlying problem is fundamentally different. In HFrEF, the heart can’t squeeze hard enough. In HFpEF, the heart squeezes fine but can’t relax and fill with blood the way it should. Think of a thick, stiff rubber ball versus a soft, weak one. Both fail to move enough blood, but for opposite reasons.
What Goes Wrong Inside the Heart
The core problem in HFpEF is diastolic dysfunction, meaning the heart struggles during its filling phase. Normally, after each contraction the heart muscle relaxes quickly, creating a low-pressure suction that draws blood in from the lungs. In HFpEF, the heart wall becomes stiff and relaxes slowly, so filling pressure rises.
At the cellular level, a giant protein called titin acts like a spring inside each heart muscle cell, controlling how easily the cell stretches. In HFpEF patients, chemical changes to titin make it stiffer than normal, increasing the resting tension in each cell. On top of that, the machinery responsible for clearing calcium out of heart cells after each contraction doesn’t work efficiently. Calcium is the trigger for muscle contraction, and when it lingers, the muscle can’t fully relax between beats.
These problems compound during physical activity. When the heart rate increases, there’s even less time for filling between beats. A heart that’s already stiff and slow to relax falls further behind, which is why exercise intolerance is often the first and most prominent symptom.
Symptoms and How They Present
The symptoms of HFpEF overlap heavily with other types of heart failure: shortness of breath, fatigue, swelling in the legs and ankles, and difficulty with physical activity. People with HFpEF tend to present with somewhat milder functional symptoms compared to those with reduced ejection fraction. They’re less likely to experience severe breathlessness at rest, episodes of waking up gasping at night, or signs of very low cardiac output.
That said, the distinction fades once people are sick enough to be hospitalized. At that point, the clinical picture looks similar regardless of ejection fraction type. The subtlety of early HFpEF symptoms is part of what makes it tricky to catch. Many patients attribute their declining exercise tolerance to aging, weight gain, or being out of shape.
Who Gets HFpEF
HFpEF is strongly linked to metabolic conditions. In a large cardiology registry analysis, 89.4% of HFpEF patients had hypertension, 55.7% were obese (BMI of 30 or higher), 71.4% had high cholesterol, and 36.8% had diabetes. The average BMI among HFpEF patients in that study was nearly 33, well into the obese range.
The typical patient is older, more often female, and carrying several of these conditions simultaneously. The metabolic burden appears to drive widespread inflammation and stiffening throughout the cardiovascular system, not just the heart. This is why some researchers describe HFpEF as a systemic disease rather than purely a heart problem.
How HFpEF Is Diagnosed
Diagnosing HFpEF is more complex than diagnosing other forms of heart failure because the hallmark measurement, ejection fraction, looks normal. Doctors rely on a combination of imaging, blood tests, and clinical scoring systems to piece together the diagnosis.
Echocardiography
An ultrasound of the heart (echocardiogram) is the primary tool. Beyond confirming a normal ejection fraction, the ultrasound looks for signs of stiff, high-pressure filling. The most studied measurement is the E/e’ ratio, which compares the speed of blood flowing into the heart with how fast the heart wall itself moves during filling. An E/e’ ratio above 9 to 10 raises suspicion for elevated filling pressures. Doctors also look at estimated pressure in the lung arteries (above 35 mmHg is significant) and the size of the left atrium, which stretches over time when filling pressures stay high.
Blood Tests
A blood marker called NT-proBNP helps support the diagnosis. Heart muscle cells release this protein when they’re under abnormal stretch. Levels vary considerably depending on whether a patient also has atrial fibrillation or kidney disease, with safety cutoffs ranging from roughly 329 to 929 pg/mL across different patient subgroups. Because of this variability, NT-proBNP works best as one piece of evidence rather than a standalone test.
Clinical Scoring Systems
Two validated scoring tools help clinicians estimate the probability of HFpEF. The H2FPEF score assigns points for six factors: a history of atrial fibrillation (3 points), obesity (2 points), taking two or more blood pressure medications (1 point), elevated lung artery pressure on ultrasound (1 point), age over 60 (1 point), and an elevated E/e’ ratio (1 point), for a maximum of 9. Higher scores indicate greater likelihood of HFpEF.
The HFA-PEFF score, developed by the European Society of Cardiology, evaluates three domains: heart function, heart structure, and biomarkers. Each domain can contribute up to 2 points, with a total possible score of 6. A score of 5 or 6 is considered diagnostic, while intermediate scores (2 to 4) may prompt additional testing, such as exercise stress echocardiography or invasive pressure measurement during a catheterization.
Treatment Options
For decades, HFpEF had no proven drug therapy. Medications that dramatically improved survival in reduced ejection fraction heart failure repeatedly failed to show benefit in HFpEF trials. That changed with a class of drugs originally developed for type 2 diabetes: SGLT2 inhibitors, which work by causing the kidneys to excrete excess sugar and fluid.
In the EMPEROR-Preserved trial, published in the New England Journal of Medicine, patients taking an SGLT2 inhibitor had a 21% lower risk of cardiovascular death or hospitalization for heart failure compared to placebo over a median follow-up of about two years. The benefit was driven primarily by a 29% reduction in heart failure hospitalizations. A second major trial, DELIVER, confirmed similar results with a different drug in the same class. These findings made SGLT2 inhibitors the first medications with strong evidence for treating HFpEF.
Beyond medication, managing the conditions that fuel HFpEF is central to treatment. Controlling blood pressure, losing weight, treating sleep apnea, and staying as physically active as possible all help reduce the burden on a stiff heart. Diuretics remain important for managing fluid retention and relieving congestion symptoms, even though they don’t change the underlying disease trajectory.
Long-Term Outlook
HFpEF carries a prognosis that many patients and even some clinicians underestimate. In a five-year population-based study, survival rates at one, three, and five years were 78%, 58%, and 43% respectively. Those numbers were dramatically worse than what would be expected for a similar-aged population without heart failure, where five-year survival was 72%. Perhaps most striking, survival in HFpEF was statistically indistinguishable from survival in reduced ejection fraction heart failure, where five-year mortality was also close to 60%.
The “preserved” in HFpEF refers only to the pumping measurement, not to the overall health of the heart or the patient’s prognosis. Early recognition, aggressive management of underlying metabolic conditions, and newer drug therapies offer the best chance of slowing progression and reducing hospitalizations.