Heart Failure
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These articles provide education to enhance your healthcare partnership. All treatment decisions should involve your healthcare team. Use this knowledge to have informed discussions, not replace medical care.
In Brief
Two people can carry the same diagnosis — heart failure — and have very different underlying problems. In one, the pumping chamber is weakened and cannot squeeze hard enough. In the other, the chamber squeezes normally but has grown stiff and cannot relax and fill. A single measurement, the ejection fraction, is what separates them, and that number shapes nearly every treatment decision that follows. The ejection fraction is also frequently misunderstood: a normal value does not mean a normal heart, and the exact cutoffs are being loosened as the field recognizes how much a single measurement can miss. This article reviews the full spectrum — reduced, mildly reduced, preserved, and improved ejection fraction — explains why the distinction changes which therapies help, and describes how the preserved form, long without a proven treatment, has begun to change.
One Diagnosis, Two Different Problems
Article 1 introduced the two ways a heart can fail: a weak squeeze, or a stiff chamber that will not fill. This distinction organizes the entire field, because the two problems call for different treatments.
The tool clinicians use to tell them apart is the ejection fraction — the percentage of blood in the heart’s main pumping chamber, the left ventricle, that is pushed out with each beat. A heart that fills with a certain amount of blood and ejects most of it has a high ejection fraction. A weakened heart that ejects only a fraction of what it holds has a low one.
When the ejection fraction is low, the problem is usually a failure of contraction — the muscle cannot squeeze forcefully enough. When the ejection fraction is normal but the person still has clear heart failure, the problem lies elsewhere: the chamber has become stiff, or fills poorly, or cannot keep up with the body’s demands despite a normal-looking squeeze. The syndrome and the symptoms of breathlessness and swelling are the same, but the underlying problem differs, and so does the treatment.
Ejection Fraction: The Number That Divides the Diagnosis — and Its Limitations
Ejection fraction is usually measured with an echocardiogram — an ultrasound scan of the heart that shows the chambers moving in real time. A healthy left ventricle ejects well over half its blood with each beat; the lower limit of normal is around 52 percent in men and 53 percent in women, and this cutoff varies with sex, age, ethnicity, and imaging method.[2] Below that, the pump is ejecting less than it should.
Two cautions matter before any number is read too confidently.
First, a normal ejection fraction does not mean a normal heart. This is a common and important misunderstanding. A person can be dangerously ill from heart failure while their ejection fraction reads a reassuring 60 percent — because their problem is stiffness and filling, not squeezing. The number measures only one aspect of the heart’s function, and it can appear normal while other aspects fail.
Second, the number itself is not as precise as it appears. The same heart, measured by two skilled people or by two different scanning methods, can yield ejection fractions several points apart, and the figure can shift with blood pressure, heart rhythm, and hydration on the day of the scan.[2] It is a useful measurement, not an exact one — which is part of why the field is moving away from treating specific cutoff numbers as fixed boundaries, as discussed at the end of this article.
With those cautions in place, the cutoffs are still how care is organized today, so they are worth knowing.
The Categories, as Clinicians Use Them Today
Current U.S. practice, set by the 2022 national heart failure guideline, sorts heart failure into four groups by ejection fraction.[1] The bands are practical tools for choosing treatment, not biological boundaries.
| Category | Ejection fraction | In plain terms |
| Reduced (HFrEF) | 40% or below | The pump is weakened; the squeeze is too weak |
| Mildly reduced (HFmrEF) | 41–49% | An in-between zone, just under normal |
| Preserved (HFpEF) | 50% or above | The squeeze looks normal, but the heart still fails — usually a stiffness and filling problem |
| Improved (HFimpEF) | Was 40% or below, now above 40% after treatment | A previously weak pump that has recovered function |
“HFrEF” and “HFpEF” are simply shorthand — heart failure with reduced or preserved ejection fraction. Roughly half of all people with heart failure fall into the preserved group, and its share is growing as populations age and conditions like obesity and diabetes become more common.[3] The two forms are close to equal in number, and increasingly different in how they are treated.
Reduced Ejection Fraction: The Weakened Pump
Heart failure with reduced ejection fraction is the form most people picture when they hear “heart failure” — a pump that has been damaged and can no longer contract with full force. This is called systolic dysfunction, a failure of the emptying phase of the heartbeat.
Its causes are usually identifiable injuries to the heart muscle: a heart attack that kills a region of muscle, long-standing high blood pressure that wears the pump down, disease of the heart muscle itself (a cardiomyopathy — literally, disease of the heart muscle), or damage from alcohol, chemotherapy, or a viral infection. Article 3 traces these routes in detail.
This form matters for treatment because its underlying mechanism is well understood. As Article 1 described, a weakened pump triggers a cascade of stress hormones — the neurohormonal cycle — that, sustained over months and years, injures the heart further. That cycle turned out to be something medicine could interrupt. Reduced ejection fraction is the form of heart failure with the strongest, clearest treatment evidence: four classes of medication, used together, measurably lower the risk of hospitalization and death.[1] Those four are the subject of Article 6. For now, the key point is that a weak-pump diagnosis comes with a clear, evidence-based treatment plan.
Preserved Ejection Fraction: More Than a Weak Squeeze
Heart failure with preserved ejection fraction is harder to explain, harder to diagnose, and — until recently — was very difficult to treat. The problem here is more complex than a weak squeeze.
The most visible piece of it is diastolic dysfunction — a failure of the filling phase. The ventricle has become thick and stiff, so it cannot relax and draw in blood easily. To fill a stiff chamber, pressure has to rise, and that elevated pressure backs up into the lungs, producing the same breathlessness seen in the reduced form. For years this was the whole story told about preserved heart failure: a stiffness problem, a “diastolic” problem.
That picture turned out to be too small. The modern understanding is that preserved-ejection-fraction heart failure is often not really a disease of the heart alone, but a whole-body condition that affects the heart.[3] The people who develop it tend to carry a cluster of other conditions — obesity, high blood pressure, type 2 diabetes, kidney disease, atrial fibrillation (an irregular heart rhythm), and the changes of aging. An influential model proposes that these conditions together create a low-grade, body-wide inflammatory state that injures the tiny blood vessels feeding the heart muscle, and that this microvascular injury — not a simple mechanical stiffness — drives the muscle to thicken, scar, and fail to relax.[4] In this understanding, the heart failure is a consequence of a body-wide metabolic problem rather than a disease that begins in the heart, and the stiff ventricle is one result of it.
This explains two things at once. It explains why preserved heart failure clusters with weight, blood sugar, and blood pressure — themes this series treats as one continuous cardiometabolic problem rather than separate diseases. And it explains the long frustration of treatment. The drugs that transformed the reduced form — the ones that quiet the neurohormonal cycle — were tested in preserved heart failure and, for years, failed to meet their goals one after another.[3] A condition driven by systemic inflammation and metabolic stress did not yield to drugs designed for a different mechanism. For a long time, a diagnosis of preserved heart failure came with good symptom management but no treatment proven to change its course.
That is the part that has finally changed — but first, the two categories in between.
The Middle and the Recovered: Mildly Reduced and Improved Ejection Fraction
Not everyone falls cleanly into “reduced” or “preserved,” and two categories capture the people in between and the people who get better.
Mildly reduced ejection fraction (41–49 percent) is the zone just below normal. People here behave, on average, somewhere between the two main groups — and a growing body of evidence suggests they respond to several of the same treatments that help the reduced form.[1] The practical trend has been to treat mildly reduced heart failure more like reduced heart failure than like preserved, and the newest thinking, described below, leans further in that direction.
Improved ejection fraction is an encouraging category, and one that is often misunderstood by patients. It describes someone whose ejection fraction was once reduced — 40 percent or below — and has climbed back above 40 percent with treatment. The pump has recovered function. The temptation, understandably, is to conclude the heart failure is cured and the medications can stop.
The evidence argues against this. In a trial that deliberately withdrew heart failure medications from people whose function had recovered, more than 40 percent relapsed within six months, their hearts weakening again once the drugs were removed.[5] The improvement, in other words, was often the treatment working, not the disease going away. This is why current guidance is to continue therapy in people with improved ejection fraction, including those who feel entirely well.[1] The recovered pump is a treated pump, and it generally needs to stay that way. It is a clear example of why some medications are worth taking consistently even when you feel fine — a point Article 6 develops.
Why the Preserved Form Has Finally Begun to Change
For decades, trials in preserved-ejection-fraction heart failure repeatedly failed to show benefit. In the last few years, that has changed, and from an unexpected direction.
The turning point came from a class of drugs first developed to lower blood sugar in diabetes: the SGLT2 inhibitors(sodium-glucose cotransporter-2 inhibitors, which cause the kidneys to excrete glucose and sodium). Two large international trials — one testing empagliflozin, one testing dapagliflozin — enrolled people with heart failure and higher ejection fractions to test whether these drugs could succeed where earlier treatments had not. Both showed that the drug reduced the combined risk of cardiovascular death or heart-failure events, a benefit driven mainly by fewer hospitalizations.[6][7] For the first time, a therapy improved a major outcome in this population. That these drugs came from diabetes research is not a coincidence: it fits the understanding of preserved heart failure as a fundamentally cardiometabolic disease. Article 11 returns to this crossover between diabetes and heart therapy.
Two further advances have widened the picture. A non-steroidal mineralocorticoid receptor antagonist (finerenone — a drug that blocks the hormone aldosterone, which drives fluid retention and scarring) was tested in people with mildly reduced and preserved ejection fraction and reduced worsening-heart-failure events compared with placebo.[8] And in people whose preserved heart failure was tied to obesity, the weight-loss drug semaglutide (a GLP-1 receptor agonist, from the same family used in diabetes and obesity) improved symptoms, physical function, and weight — treating the metabolic driver rather than the heart directly.[9] Neither of these newer therapies clearly reduced deaths, and each applies to particular patients rather than everyone; their value is real but specific.
In summary, preserved-ejection-fraction heart failure went from having no proven disease-modifying treatment to having several within a few years. The effects so far are mostly on hospitalizations and symptoms rather than on survival, and which therapy fits which person depends on the individual’s other conditions and belongs with their care team. This is meaningful progress rather than a cure: a real and expanding set of options where there previously were none.
The Field Is Moving Beyond Rigid Cutoffs
One last shift is worth knowing, because it will shape how heart failure is described in the coming years. In 2026, the international bodies that define heart failure issued an updated consensus that deliberately steps back from rigid ejection-fraction cutoffs.[2] Instead of fixed numeric cutoffs, it groups heart failure into three trajectory-based categories — reduced, preserved, and improved — and emphasizes that a person’s ejection fraction can change with treatment and over time, and that a single measurement varies with how and when it is taken.
The reasoning is exactly the two cautions from earlier in this article: the number is imprecise, and it changes. Treating 40 percent and 41 percent as fundamentally different diseases never made biological sense, and evidence increasingly shows that people with slightly reduced function benefit from the therapies that help the clearly reduced group.[2] A new national treatment guideline built on this framework is expected in the years ahead. For a patient, the practical meaning is reassuring rather than confusing: your category is not a permanent label, treatment follows your heart’s trajectory rather than a single snapshot, and the boundaries are being drawn to match how the disease behaves.
Clinical Bottom Line
Heart failure divides into two broad problems that happen to share a name: a weakened pump that cannot squeeze (reduced ejection fraction) and a stiff, poorly filling heart that usually reflects a whole-body cardiometabolic condition (preserved ejection fraction), with mildly reduced and improved categories in between. The distinction is not academic — it determines which treatments help. The reduced form has four medication classes with strong evidence behind them. The preserved form, long untreatable, now has a real and growing set of options, several of them borrowed from diabetes and obesity medicine, reflecting its metabolic roots. A normal ejection fraction never rules heart failure out, the exact cutoffs are being loosened because they proved too rigid, and a recovered ejection fraction usually needs continued treatment to stay recovered. Whatever the category, rapidly worsening breathlessness or swelling deserves prompt evaluation rather than waiting — Article 10 covers how to tell an early drift from an emergency.
Knowing which form you have is the first step in understanding why your treatment plan looks the way it does — and why it may differ, reasonably, from someone else who carries the same diagnosis.
What Comes Next
This article sorted heart failure by what the pump is doing now. Article 3 asks how it got there: the roads into heart failure — prior heart attacks, long-standing high blood pressure, valve disease, diabetes, and disorders of the heart muscle itself — how each injures the heart over time, and why some of that injury can be slowed or partly reversed when caught early.
Key Terms
Ejection fraction: The percentage of blood in the left ventricle that is pumped out with each beat. Normal is more than about 50 percent. It measures the strength of the squeeze, not everything the heart does.
Echocardiogram: An ultrasound scan of the heart that shows the chambers moving in real time; the usual way ejection fraction is measured.
Systolic dysfunction: A failure of the heart’s emptying (contracting) phase — a weak squeeze. The core problem in reduced-ejection-fraction heart failure.
Diastolic dysfunction: A failure of the heart’s filling (relaxing) phase — a stiff chamber that will not fill easily. A central feature of preserved-ejection-fraction heart failure.
HFrEF (heart failure with reduced ejection fraction): Heart failure with an ejection fraction of 40 percent or below; a weakened pump.
HFmrEF (heart failure with mildly reduced ejection fraction): Heart failure with an ejection fraction of 41–49 percent; an in-between zone increasingly treated like the reduced form.
HFpEF (heart failure with preserved ejection fraction): Heart failure with an ejection fraction of 50 percent or above; the squeeze looks normal, but the heart still fails, usually a stiffness-and-filling problem tied to whole-body conditions.
HFimpEF (heart failure with improved ejection fraction): Heart failure in someone whose ejection fraction was once reduced and has recovered above 40 percent with treatment; still requires ongoing therapy.
Cardiomyopathy: Disease of the heart muscle itself, from causes such as genetics, viral infection, alcohol, or chemotherapy.
Atrial fibrillation: A common irregular, often rapid heart rhythm that frequently accompanies preserved heart failure.
Microvascular: Relating to the smallest blood vessels; microvascular injury to the vessels feeding the heart muscle is part of the modern model of preserved heart failure.
SGLT2 inhibitor: A drug class (for example, empagliflozin, dapagliflozin) first developed for diabetes that causes the kidneys to excrete glucose and sodium; the first therapy shown to improve outcomes across the higher-ejection-fraction range.
Mineralocorticoid receptor antagonist (MRA): A drug that blocks aldosterone, a hormone that drives fluid retention and scarring in the heart; finerenone is a newer non-steroidal example studied in preserved heart failure.
GLP-1 receptor agonist: A drug class (for example, semaglutide) used for diabetes and obesity; studied in obesity-related preserved heart failure, where it improved symptoms and function.
References
- Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2022;145:e895–e1032. https://doi.org/10.1161/CIR.0000000000001063
- Walsh MN, Kober L, Sliwa K, et al. AHA/ACC/ESC/WHF Expert Consensus Document: Second Universal Definition of Heart Failure (2026). Circulation. 2026;153. https://doi.org/10.1161/CIR.0000000000001455
- Redfield MM, Borlaug BA. Heart Failure With Preserved Ejection Fraction: A Review. JAMA. 2023;329(10):827–838. https://doi.org/10.1001/jama.2023.2020
- Paulus WJ, Tschöpe C. A Novel Paradigm for Heart Failure With Preserved Ejection Fraction: Comorbidities Drive Myocardial Dysfunction and Remodeling Through Coronary Microvascular Endothelial Inflammation. J Am Coll Cardiol. 2013;62(4):263–271. https://doi.org/10.1016/j.jacc.2013.02.092
- Halliday BP, Wassall R, Lota AS, et al. Withdrawal of pharmacological treatment for heart failure in patients with recovered dilated cardiomyopathy (TRED-HF): an open-label, pilot, randomised trial. Lancet. 2019;393(10166):61–73. https://doi.org/10.1016/S0140-6736(18)32484-X
- Anker SD, Butler J, Filippatos G, et al. Empagliflozin in Heart Failure with a Preserved Ejection Fraction (EMPEROR-Preserved). N Engl J Med. 2021;385(16):1451–1461. https://doi.org/10.1056/NEJMoa2107038
- Solomon SD, McMurray JJV, Claggett B, et al. Dapagliflozin in Heart Failure with Mildly Reduced or Preserved Ejection Fraction (DELIVER). N Engl J Med. 2022;387(12):1089–1098. https://doi.org/10.1056/NEJMoa2206286
- Solomon SD, McMurray JJV, Vaduganathan M, et al. Finerenone in Heart Failure with Mildly Reduced or Preserved Ejection Fraction (FINEARTS-HF). N Engl J Med. 2024;391(16):1475–1485. https://doi.org/10.1056/NEJMoa2407107
- Kosiborod MN, Abildstrøm SZ, Borlaug BA, et al. Semaglutide in Patients with Heart Failure with Preserved Ejection Fraction and Obesity (STEP-HFpEF). N Engl J Med. 2023;389(12):1069–1084. https://doi.org/10.1056/NEJMoa2306963
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