The short answer#
Two people can carry the same diagnosis of heart failure, sit in the same clinic with the same breathlessness and swollen ankles, and yet need almost opposite treatment plans. What separates them is one number: the ejection fraction, or the fraction of blood the left ventricle pushes out with each beat. The 2022 guideline from the American Heart Association, American College of Cardiology, and Heart Failure Society of America uses that number to divide heart failure into groups. When the fraction is 40 percent or below, it is called heart failure with reduced ejection fraction (HFrEF). When it is 50 percent or above, it is heart failure with preserved ejection fraction (HFpEF). The reduced type has a proven set of medicines that lengthen life. The preserved type is harder to diagnose and, until recently, had far less to offer.
Key points#
- Ejection fraction is the percentage of blood the left ventricle ejects per beat; a healthy heart is usually around 55 to 70 percent.
- The guideline uses four bands: reduced (40 percent or below), mildly reduced (41 to 49), preserved (50 or above), and improved (once reduced, now recovered).
- HFrEF is a squeezing problem; HFpEF is a filling and relaxing problem. Both cause the same symptoms.
- HFrEF has four drug classes with strong survival evidence. HFpEF has fewer, with SGLT2 inhibitors the best supported so far.
- Knowing which band you fall into tells you which evidence, and which treatments, apply to you.
Two ways a pump can fail#
Picture the left ventricle as a pump built from muscle. It has to do two jobs in sequence: fill with blood, then squeeze that blood out to the body. Heart failure can start on either side of that cycle.
In HFrEF, the squeeze is the problem. The muscle has weakened and cannot contract with enough force, so less blood leaves the heart with each beat. This is a failure of systole, the contracting phase.
In HFpEF, the squeeze looks fine but the fill does not. The ventricle has grown stiff and cannot relax and expand the way it should between beats, so it takes higher pressure to load it with blood, and that pressure backs up into the lungs. This is a failure of diastole, the relaxing and filling phase. Think of a thick, rigid balloon that resists being inflated versus a thin, floppy one that fills easily but cannot snap back to push its contents out. Same shortness of breath and fluid buildup for the patient, two different mechanical faults inside the pump.
Reading the ejection fraction bands#
The guideline turns that single percentage into four categories:
- Reduced (HFrEF): ejection fraction of 40 percent or lower.
- Mildly reduced (HFmrEF): 41 to 49 percent.
- Preserved (HFpEF): 50 percent or higher, with objective proof that filling pressures inside the heart are elevated.
- Improved (HFimpEF): a fraction that was once 40 percent or below and has climbed above 40 percent with treatment.
That last band matters because it reframes the whole idea. These labels are not permanent addresses. People move between them, and someone whose heart recovers still generally needs to continue the therapy that got them there.
Why the preserved type hides#
A weak squeeze is easy to catch. An echocardiogram measures the ejection fraction directly, so HFrEF tends to announce itself on the first scan. HFpEF is quieter. The ejection fraction reads normal and the heart may look structurally unremarkable at rest, which means the diagnosis depends on proving that filling pressures are high despite an ordinary-looking squeeze.
Blood tests do not always close the case. Natriuretic peptides, the hormones a stretched heart releases, tend to run lower in HFpEF than in HFrEF. In people carrying extra weight, a frequent companion of HFpEF, those peptides can dip below the usual cutoff even when pressures measured directly inside the heart are clearly elevated. A normal result does not rule the condition out.
To bridge that uncertainty, clinicians use structured probability tools. The H2FPEF score, for example, weighs body mass index, high blood pressure, atrial fibrillation, older age, and ultrasound estimates of filling pressure. When the score lands in a middle zone, the more definitive move is to measure pressures during exercise, sometimes with a catheter, because a heart that behaves at rest can reveal high pressures the moment it is asked to work. That is a far heavier lift than reading an ejection fraction once, and it helps explain why HFpEF is so often missed.
Why the treatments diverge#
Here the two types part ways most sharply. For HFrEF, decades of trials settled on what clinicians call the four pillars of guideline-directed therapy: beta blockers, mineralocorticoid receptor antagonists, angiotensin receptor-neprilysin inhibitors, and sodium-glucose cotransporter-2 (SGLT2) inhibitors. Each acts on the neurohormonal signaling that pushes a weakened heart to remodel and decline, and each adds its own survival benefit. Taken together, they meaningfully cut both death and hospital admissions.
That same strategy mostly stumbled in HFpEF. Medicines that plainly extended life when the ejection fraction was reduced did not repeat those survival gains when it was preserved, and the 2022 guideline mirrors that in the strength of its wording. SGLT2 inhibitors carry the firmest recommendation for HFpEF, a Class 2a, supported by trials such as EMPEROR-Preserved, in which empagliflozin lowered the combined risk of cardiovascular death or heart failure hospitalization, mainly by keeping people out of the hospital. Mineralocorticoid receptor antagonists and angiotensin receptor-neprilysin inhibitors sit lower at Class 2b. Even the SGLT2 benefit here has leaned toward fewer admissions rather than the clear reduction in all-cause death that the four pillars deliver in HFrEF.
Why the gap? HFpEF is not one disease with one cause. It tangles together obesity, high blood pressure, kidney disease, and inflammation, and no single lever moves all of it. A drug that helps one subset of patients may do little for another, which washes out the average effect in a large trial. The reduced-EF population is more mechanistically consistent, so trials could aim at a shared pathway and hit it repeatedly. This is a recurring theme in chronic-disease research: a syndrome defined by shared symptoms can hide very different biology underneath, and careful appraisal of trial populations is what keeps treatment honest.
What it means for you#
The ejection fraction band is not paperwork. It decides which evidence is yours to use. If your fraction is reduced, there is a defined, life-extending regimen worth building up to full doses with your clinician. If it is preserved, the diagnosis itself may take more effort to confirm, the treatable drivers such as blood pressure and body weight carry more weight, and SGLT2 inhibitors have become the best-supported medicine even as the research keeps maturing. Knowing your number, and which side of the line it puts you on, is where an informed conversation with your cardiologist begins.
Sources and further reading
Questions and answers
Can heart failure move from one type to another?
Yes. Someone with a reduced ejection fraction who responds well to treatment can recover into the improved category, and progression can also shift a person's classification over time. That is why follow-up scans and staying on effective therapy both matter.
Is preserved ejection fraction a milder form of heart failure?
No. A normal ejection fraction does not mean a mild illness. HFpEF carries real symptoms, hospital risk, and shortened survival; it is simply harder to diagnose and, so far, has fewer treatments with strong outcome evidence.
Why do the same drugs not work for both types?
HFrEF is driven largely by neurohormonal signaling that several drug classes can interrupt. HFpEF stems from a stiff, poorly relaxing heart tied to a mix of conditions, so a single mechanism rarely captures it, and trial results in HFpEF have been more modest as a result.