Heart failure with preserved ejection fraction, usually shortened to HFpEF, means the heart still squeezes normally and pushes out 50% or more of the blood inside its main chamber, while the muscle has become stiff and no longer relaxes and fills as it should, which causes breathlessness, tiredness and swelling [8,9].
This page provides general information. It does not replace advice from a doctor or another qualified healthcare professional.
Heart failure means the heart cannot pump blood around the body as well as it should. It does not mean the heart has stopped [1,2].
What ejection fraction measures. The left ventricle is the heart’s main pumping chamber. It never empties fully, so doctors measure the share of blood inside it pushed out with each squeeze. A normal heart pushes out 55% to 70%, and heart failure is grouped by that number [2,7,8]:
The part people find hardest. In HFpEF the squeeze is normal. The trouble is the other half of each beat, when the muscle should relax and the chamber refill. It has grown thick and stiff and holds less blood than usual, so the percentage stays normal while the amount reaching the body is not enough [8,9]. The older name is diastolic heart failure, after diastole, the filling part of the beat [9]. The reduced form, where the muscle squeezes weakly, has its own trialport guide [8].
If your scan was called normal, that is a common place to be, since the pumping measure really is normal [8]. A firm diagnosis is hard to make [11], and guidelines now ask for separate evidence that pressure inside the heart is raised [5,7].
Between 1% and 2% of adults have heart failure of all kinds, rising from about 1% under 55 to more than 10% over 70. These count people already diagnosed, so the true number is likely higher [5].
About half of all heart failure is thought to be the preserved or mildly reduced form, mainly from studies in hospital [5]. In a 15-year hospital series ending in 2001 the share that was the preserved form rose steadily while survival improved only for the reduced form [12]. People with HFpEF are typically older, and more are women [5]. About 6.7 million adults in the United States have heart failure, projected to reach 11.4 million by 2050 [19].
HFpEF is better thought of as the end point of several conditions than as one disease [14]. Most causes are long-term health conditions rather than anything inherited [5].
Causes worth ruling out. Cardiac amyloidosis, hypertrophic cardiomyopathy, valve disease and advanced kidney failure can look like HFpEF and need different treatment [14]. Amyloidosis, a build-up of abnormal protein in the muscle, is easily missed: one study of 120 people admitted with HFpEF and a thickened left ventricle found it in 13% [13]. Our guide to ATTR-CM covers it in full.
Genes. A gene is an instruction the body uses to build and run itself. Most HFpEF is not inherited, meaning not passed down through families, though hypertrophic cardiomyopathy and one form of transthyretin amyloidosis can be, and genetic testing tells that form apart [7].
The main symptoms are the same as in other kinds of heart failure [1,2]:
Exercise intolerance is often the dominant problem, with many people managing at rest and hitting a wall as soon as they do something, and naming physical functioning as the limitation they notice most [15,20]. Signs a doctor can see may be absent early [5,6].
When to seek urgent help. In the United Kingdom, ask for an urgent doctor’s appointment or contact NHS 111 if you become breathless lying down or during everyday activity, cough up frothy pink phlegm, or gain weight suddenly [1]. A sudden unexpected weight gain of more than 2 kg over about three days usually means fluid building up, and heart failure teams often ask people to alert them or adjust their water tablet [5]. Call 999, or 911 in the United States, for severe difficulty breathing, gasping or choking, lips or skin turning pale, blue or grey, or if someone passes out [1].
A family doctor takes a history, examines you and arranges tests, then refers you to a heart specialist. A chest X-ray, heart tracing and breathing tests help rule out other causes of breathlessness [1,3].
The blood test, and its important limitation. Natriuretic peptides are substances the heart releases under strain, and raised levels support the diagnosis: above 125 pg/mL for NT-proBNP or 35 pg/mL for BNP [5]. Levels run lower in HFpEF than in the reduced form, and up to 20% of people whose HFpEF is confirmed by pressure measurements fall below the thresholds, particularly if they carry extra weight, since fat tissue clears these substances faster [5]. Common heart medicines lower the reading too [3], so a normal result does not rule it out [11].
The scan looks past the ejection fraction. An echocardiogram, an ultrasound of the heart, also measures filling: the size of the left atrium, the thickness of the muscle wall, and how fast blood enters compared with how fast the muscle relaxes. The more of these are abnormal, the more likely HFpEF is [5].
Two scores, in plain language. The H2FPEF score turns six simple facts, including age over 60, obesity and atrial fibrillation, into a total from 0 to 9, with the odds roughly doubling per point [10]. HFA-PEFF works in four steps: symptoms and simple tests, a scored scan and blood test, exercise testing, then a search for a specific cause [11]. Both leave many people in an uncertain middle band [5]. Where doubt remains, the confirming test measures pressure inside the heart during exercise through a fine tube, used mainly in research [5].
There is no cure [1,2]. Treatment eases symptoms, treats what is driving it and reduces the chance of hospital admission.
The honest part. For years nothing had been shown to reduce death or serious events in HFpEF, and large trials of medicines that work well in the reduced form all missed their main goals [5]. That has changed.
SGLT2 inhibitors came first. Dapagliflozin and empagliflozin, first developed for diabetes, make the kidneys pass out more sugar and salt. Two trials in nearly 12,000 people with an ejection fraction above 40% both reduced their main measure, by about 20% combined, driven by 26% fewer hospital stays, with no clear reduction in death from heart causes, with or without diabetes [6]. European guidance now gives this its strongest recommendation [6], the United States guideline says it can be beneficial [7], and NICE recommends both in England [4,22].
Finerenone is the newer addition. It blocks aldosterone, a hormone that makes the body hold on to salt and water. In 6,001 people with an ejection fraction of 40% or more it cut the combined count of worsening heart failure events and death from heart causes by 16%, though high potassium was more common [17]. The United States regulator approved it for this group in July 2025 [18]. Spironolactone works on the same hormone and is used selectively at the lower end of the range [5,7].
Water tablets such as furosemide relieve congestion, usually at a low to medium dose in HFpEF, and treating the cause and other conditions present carries the strongest recommendation [3,5,6].
Exercise is recommended for everyone with heart failure who is able, to improve exercise capacity and quality of life and reduce hospital stays [5]. Pooling six randomized trials in people with an ejection fraction of 50% or above, physical functioning improved clearly [20]. Everyone diagnosed should be offered a personalized, exercise-based rehabilitation program [1,3].
GLP-1 receptor agonists. In 529 people with HFpEF and a body-mass index of 30 or above, weekly semaglutide over 52 weeks improved symptoms, physical limitation and walking distance more than placebo, and lowered weight and a marker of inflammation. It measured how people felt and moved rather than survival, and at publication no treatment had been approved specifically for obesity-related HFpEF [15].
Care is shared between a specialist heart failure team and a family doctor, with a review at least every six months and a written care plan [3,5]. Weigh yourself regularly, since fluid shows on the scales first [1,2]. Guidance in England says clinicians should not routinely tell people with heart failure to restrict salt or fluid, and should advise only where intake is high or blood sodium is low [3]. Have the vaccinations you are offered, discuss pregnancy if relevant, and tell the licensing authority if you drive [1,3].
Anxiety about the future is common and normal, and a cardiac nurse helpline and self-referral talking therapies are available [1,2]. If symptoms keep worsening, ask about palliative care, which is about controlling symptoms and living better [1,3]. Predicting the course for one person is uncertain, and English guidance asks clinicians to be frank about that [3].
Clinical trials test whether a treatment works and is safe. HFpEF research is unusually active. Deciding whether to look into a study is personal, and it helps to take it in steps.
Worth being clear on what a study involves:
Every trial has rules about who can take part, called eligibility criteria. For an HFpEF study they might include an ejection fraction at or above a set figure such as 50% or 40%, symptoms of a particular severity, a natriuretic peptide level above a set threshold, changes on the scan such as a thickened muscle or enlarged left atrium, taking a water tablet already, kidney function and potassium within limits, a body-mass index threshold in weight-related studies, and not being pregnant.
trialport’s medifit helps people consider information related to possible medical suitability. It does not diagnose a condition, confirm eligibility or replace formal screening by the study team.
Explore heart failure with preserved ejection fraction clinical trials through trialport
A study can look right on paper and still be hard in practice:
trialport’s readifit helps people reflect on their understanding, motivation, time, routines, support, emotions and practical arrangements.
Useful questions to put to a research team:
Taking part is voluntary. A person can ask questions, speak with people they trust and choose not to participate.
Search for clinical trials at app.trialport.com.
Study status checked: 3 August 2026. Research moves quickly, so this list will date. For current information, search at app.trialport.com.
Few countries have an organization for HFpEF specifically, so elsewhere the clinic is the best route.
My scan was normal, so how can I have heart failure?
A normal ejection fraction does not rule it out: the pumping share really is normal in HFpEF. The stiffened muscle does not relax and fill properly, so the blood reaching your body is still not enough [5,7,8].
Is HFpEF less serious than the reduced form?
Not in the way people assume. Most observational studies show the difference in survival is negligible, and survival improved over time for the reduced form but not the preserved form [5,12].
Does a normal blood test mean I do not have it?
No. Levels are lower in HFpEF, and up to 20% of people with confirmed HFpEF fall below the threshold, particularly if they carry extra weight [5,11].
Is this my fault because of my weight?
No. Obesity is one of several conditions that contribute, alongside high blood pressure, diabetes, atrial fibrillation, kidney disease and aging, and it is biology rather than a moral failing [5,21]. Treatments that lower weight, and exercise training, improve symptoms and what people can do [15,20].
What treatment should I expect?
An SGLT2 inhibitor, a water tablet if you are retaining fluid, treatment for your other conditions, finerenone where suitable, and an offer of exercise-based rehabilitation [1,4,6,7,17].
Could something else be causing it?
Sometimes, and it is worth asking. Cardiac amyloidosis, hypertrophic cardiomyopathy and valve disease can look like HFpEF and need different treatment [13,14].
Written by: trialport editorial team
Reviewed by: Keith Berelowitz, Founder and CEO, trialport
Reviewed on: 3 August 2026
Next review due: 3 August 2027
References last checked: 3 August 2026