Heart Failure: The 4 Types and How to Treat Each One

The Problem You Already Know Too Well

You walk into a room and the patient is short of breath, ankles swollen to the knees, and tired. The chest X-ray shows cephalization and Kerley B lines. The echo says LVEF 35 percent. Heart failure. Again.

Except this time the echo says LVEF 58 percent. And the patient is still drowning in fluid. So... what exactly are you treating?

Heart failure is no longer just one disease with one treatment algorithm. The 2022 ACC/AHA/HFSA guidelines formalized something we already knew from the bedside: heart failure comes in at least four flavors, and each one demands a different approach. Getting this right matters. One in four Americans will develop heart failure in their lifetime, and the number of people living with it is climbing toward 11 million by 2050.

Let me walk you through the four types, how to tell them apart, and what to actually do about each one.

The Four Types

HFrEF: The Classic Reduced Fraction

Heart failure with reduced ejection fraction. LVEF at or below 40 percent. This is the form we know best because it has been studied the longest, and the evidence base is massive.

Think of HFrEF as a pump problem. The left ventricle dilated, thinned, and lost contractile force. The most common causes are ischemic cardiomyopathy from coronary artery disease and nonischemic dilated cardiomyopathy (viral, genetic, toxic, or idiopathic).

The clinical picture is textbook: dyspnea on exertion progressing to orthopnea and paroxysmal nocturnal dyspnea, bilateral crackles, elevated JVP, peripheral edema. BNP is elevated. Chest X-ray shows cardiomegaly with pulmonary congestion.

HFmrEF: The Gray Zone

Heart failure with mildly reduced ejection fraction. LVEF between 41 and 49 percent plus evidence of elevated left ventricular filling pressures.

This is the uncomfortable middle ground. It is not quite HFrEF, not quite HFpEF, and for a long time we had very little evidence to guide treatment. Recent data suggest that HFmrEF patients share characteristics of both neighboring phenotypes, and many of the therapies proven in HFrEF and HFpEF now extend into this range.

HFpEF: The Preserved Fraction Puzzle

Heart failure with preserved ejection fraction. LVEF at or above 50 percent with evidence of spontaneous or provokable elevated left ventricular filling pressures.

This is the hardest diagnosis you will make in cardiology. The pump number looks fine, but the heart is stiff. It cannot relax properly during diastole, so filling pressures shoot up even though systolic function is preserved. The patient has all the symptoms of heart failure but a reassuring echo number.

HFpEF is the fastest-growing form of heart failure, and its incidence has nearly doubled over the past two decades. It tends to affect older patients, more often women, with significant comorbidities: hypertension, diabetes, obesity, atrial fibrillation, chronic kidney disease. The H2FPEF score helps you at the bedside:

• BMI greater than 30 kg/m² (2 points)
• Hypertension on two or more medications (1 point)
• Atrial fibrillation, paroxysmal or persistent (3 points)
• Pulmonary artery systolic pressure above 35 mmHg on echo (1 point)
• Age over 60 years (1 point)
• E/e' ratio greater than 9 on echo (1 point)

A score of 6 or higher has 97 percent specificity for HFpEF. A score of 0 to 1 effectively rules it out.

HFimpEF: The New Kid

Heart failure with improved ejection fraction. This is a brand-new classification in the 2022 guidelines. It describes patients who previously had HFrEF (LVEF at or below 40 percent) and now have a follow-up LVEF greater than 40 percent.

This matters because it captures a real clinical phenomenon: many patients recover systolic function with aggressive guideline-directed medical therapy. Tachycardia-mediated cardiomyopathy, peripartum cardiomyopathy, and alcohol-induced cardiomyopathy are classic examples where EF can normalize. Recognizing HFimpEF helps you decide whether to continue, de-escalate, or adjust therapies.

Treating HFrEF: The Four Pillars

If you take nothing else away from this post, remember this: the four pillars of HFrEF treatment should be started together, not one at a time. The 2024 ACC Expert Consensus Decision Pathway made this crystal clear.

Pillar One: SGLT2 Inhibitors

Dapagliflozin and empagliflozin. Originally diabetes drugs, now foundational heart failure therapy regardless of whether the patient has diabetes. They reduce cardiovascular mortality and heart failure hospitalizations through multiple mechanisms: osmotic diuresis reducing preload, improved myocardial metabolism shifting from fatty acid to glucose oxidation, and favorable effects on cardiac structure.

Dapagliflozin 10 mg daily or empagliflozin 10 mg daily. Start it early. Do not wait for the other three pillars to be titrated.

Pillar Two: ARNI

Sacubitril/valsartan replaces the ACE inhibitor or ARB position. The PARADIGM-HF trial showed it was superior to enalapril in reducing cardiovascular death and heart failure hospitalization. It works by blocking the angiotensin II receptor while simultaneously inhibiting neprilysin, which increases natriuretic peptides, vasodilation, and sodium excretion.

There is a caveat: you need a 36-hour washout period if switching from an ACE inhibitor to avoid angioedema. Start at 24/26 mg twice daily and titrate to 97/103 mg twice daily as tolerated.

Pillar Three: Evidence-Based Beta-Blockers

Not all beta-blockers are equal in heart failure. Only three have mortality benefit in HFrEF: bisoprolol, carvedilol, and metoprolol succinate extended-release. Metoprolol tartrate does not count. Nebivolol does not count (at least not in the US evidence base).

Start low and go slow, but actually do go. Carvedilol 3.125 mg twice daily up to 25 mg twice daily. Bisoprolol 1.25 mg daily up to 10 mg daily. Metoprolol succinate ER 25 mg daily up to 200 mg daily.

Pillar Four: Mineralocorticoid Receptor Antagonists

Spironolactone or eplerenone. The RALES and EMPHASIS-HF trials established these as mortality-reducing therapy in HFrEF. They block aldosterone-mediated fibrosis, sodium retention, and potassium wasting.

Spironolactone 12.5 to 25 mg daily. Eplerenone 25 to 50 mg daily. Monitor potassium and renal function within one week of starting and again at one month.

The Strategy: Four at Once

Here is the paradigm shift. Instead of starting one drug, titrating it over months, then adding the next, the current recommendation is to initiate all four classes at low doses simultaneously in stable patients. Target doses within two to three months. Multiple studies show this approach gets patients to protective doses faster without increasing adverse events.

Treating HFpEF: Finally Some Answers

For decades, HFpEF treatment was essentially "diuretics and good wishes." That changed dramatically in the last two years.

SGLT2 Inhibitors: The Cornerstone

Dapagliflozin (DELIVER trial) and empagliflozin (EMPEROR-Preserved trial) both showed significant reduction in cardiovascular death and heart failure hospitalization in HFpEF. This is a Class 2a recommendation. Start an SGLT2 inhibitor in every HFpEF patient unless contraindicated.

Finerenone: The Game Changer

In July 2025, the FDA approved finerenone (Kerendia) for heart failure with LVEF at or above 40 percent. The FINEARTS-HF trial showed a significant reduction in the composite of cardiovascular death and total heart failure events. Finerenone is a nonsteroidal, selective MRA with potentially fewer endocrine side effects than spironolactone.

This is huge for HFpEF, which has historically had very few disease-modifying therapies.

GLP-1 Receptor Agonists: The Obesity Connection

The obesity-HFpEF link is now being treated directly. Semaglutide and tirzepatide have shown improved symptoms, physical function, and reduced cardiovascular events in obese HFpEF patients through the STEP-HFpEF and SUMMIT trials. The 2025 CCS/CHFS guidelines now recommend GLP-1 receptor agonists for symptomatic patients with LVEF at or above 45 percent and BMI at or above 30 kg/m².

ARNI and MRA: Secondary Options

Sacubitril/valsartan has a Class 2b recommendation in HFpEF. It may be particularly useful in women or patients with LVEF between 45 and 57 percent. Spironolactone also has a Class 2b recommendation for symptomatic HFpEF based on the TOPCAT trial data.

Treating HFmrEF: Borrowing from Both Sides

Since HFmrEF sits between HFrEF and HFpEF, you can borrow therapies from both. The four pillars of HFrEF treatment extend into this range, and the SGLT2 inhibitor data from both DELIVER and EMPEROR-Preserved cover patients with mildly reduced EF. Treat it aggressively, because many HFmrEF patients will progress to HFrEF without intervention.

Treating HFimpEF: Do Not Stop Everything

This is where residents make mistakes. The EF improved, so you stop all the medications. Then the EF drops again three months later and the patient ends up in the ICU.

HFimpEF patients should generally continue guideline-directed medical therapy. The improvement in EF is often a result of the treatment itself. De-escalation can be considered selectively, but abrupt discontinuation is dangerous. Continue close follow-up with repeat echocardiography at six to twelve months.

When Medical Therapy Is Not Enough

Despite optimal medical therapy, some patients progress to advanced heart failure. Recognizing when to refer matters.

Device Therapy

An ICD is indicated for primary prevention when LVEF remains at or below 35 percent despite at least three months of guideline-directed medical therapy (or 40 days post-MI). Cardiac resynchronization therapy with a defibrillator (CRT-D) adds value when the QRS duration is 120 ms or greater, particularly with left bundle branch block morphology.

LVAD and Transplant Referral

Refer to an advanced heart failure center when you see any of these red flags:

• Peak VO₂ below 12 mL/kg/min on cardiopulmonary exercise testing
• Three or more heart failure hospitalizations in the past year without a clear precipitant
• Dependence on continuous intravenous inotropic therapy
• Progressive end-organ dysfunction (worsening renal or hepatic function from low cardiac output, not volume overload)
• Severe hemodynamic compromise: pulmonary capillary wedge pressure at or above 20 mmHg with systolic blood pressure at or below 80 to 90 mmHg

Do not wait for irreversible organ damage. Early referral gives the transplant team time to evaluate and optimize.

The Clinical Bottom Line

Heart failure is not one disease. It is four distinct entities that happen to share symptoms of fluid overload and low cardiac output. The LVEF number on that echo is your first branching point, but it is not the end of the story.

For HFrEF, start all four pillars early and titrate aggressively. For HFpEF, an SGLT2 inhibitor is now your anchor therapy, with finerenone and GLP-1 receptor agonists joining the arsenal. For HFmrEF, treat it like HFrEF until proven otherwise. For HFimpEF, keep the medications running.

The epidemiology is not on our side. One in four people will develop heart failure. But the treatment landscape has never been stronger. Use what you have, start early, and refer before it is too late.