Whether a person can increase their Ejection Fraction (EF) is a common question for those diagnosed with heart failure, and the answer is frequently positive. Ejection Fraction is the percentage of blood leaving the heart with each contraction; a low percentage signals inefficient pumping. This condition, often termed heart failure with reduced ejection fraction, requires a coordinated and sustained treatment approach. Improvement is often possible through medical intervention, advanced device therapy, and dedicated lifestyle changes.
Understanding Ejection Fraction
Ejection Fraction quantifies the efficiency of the heart’s main pumping chamber, the left ventricle. It is calculated by dividing the amount of blood pumped out by the total volume inside the ventricle before contraction, expressed as a percentage. A normal EF is between 50% and 70%.
An EF between 41% and 49% is considered mildly reduced or borderline. A reading of 40% or less is classified as heart failure with reduced ejection fraction (HFrEF). The most common measurement method is an echocardiogram, a non-invasive ultrasound of the heart.
A low EF indicates the heart muscle is weakened and cannot contract forcefully enough to push out sufficient blood. The goal of HFrEF therapy is to reduce chronic stress and promote “reverse remodeling”—the process where the enlarged ventricle returns to a more normal size and shape. When the EF improves from 40% or less to over 40%, it is sometimes referred to as heart failure with improved ejection fraction.
Pharmacological Treatments to Improve Output
Improving heart function and EF primarily involves Guideline Directed Medical Therapy (GDMT). These drugs counteract overactive hormonal systems that damage the failing heart, reducing the heart’s workload and allowing the muscle to recover strength.
One cornerstone involves Angiotensin Receptor-Neprilysin Inhibitors (ARNIs), often preferred over older ACE inhibitors or ARBs. ARNIs block harmful neurohormonal activity while preventing the breakdown of beneficial natural peptides. This dual action relaxes blood vessels and helps excrete excess sodium and water, proving superior in reducing cardiovascular death and hospitalization.
Beta-blockers are another foundational treatment. They dampen the effects of the sympathetic nervous system, which is overstimulated in heart failure. By slowing the heart rate and reducing contraction force, these medications allow the heart to fill more completely. Consistent use promotes the reverse remodeling necessary for EF improvement over time.
Mineralocorticoid Receptor Antagonists (MRAs), such as spironolactone and eplerenone, block the effects of the hormone aldosterone. Aldosterone contributes to fluid retention, inflammation, and scar tissue formation (fibrosis) in the heart muscle. MRAs counteract these damaging effects, protecting the heart and improving outcomes.
The fourth class is Sodium-Glucose Cotransporter-2 (SGLT2) inhibitors. These drugs provide significant cardiovascular benefits, even for non-diabetic patients. They primarily work in the kidney to reduce volume overload and may also have direct cardioprotective effects on the heart muscle.
Device Therapy and Surgical Options
When medication is insufficient, or when electrical or structural issues exist, devices and surgical procedures support or restore heart function.
One common intervention is Cardiac Resynchronization Therapy (CRT). This is used when the ventricles do not contract simultaneously (electrical dyssynchrony). A CRT device, a specialized pacemaker, sends electrical impulses to both ventricles simultaneously, forcing coordinated contraction. This significantly enhances pumping efficiency, increasing EF and reducing heart failure symptoms.
For patients with a low EF (35% or less), there is an increased risk of sudden cardiac death from rapid heart rhythms. An Implantable Cardioverter-Defibrillator (ICD) monitors the heart’s rhythm and delivers an electrical shock if a life-threatening arrhythmia occurs. ICDs are often combined with CRT (CRT-D) for both rhythm correction and resynchronization.
Surgical procedures like coronary revascularization—including percutaneous coronary intervention (PCI) or Coronary Artery Bypass Grafting (CABG)—may be recommended if the low EF is caused by blocked arteries. Restoring blood flow to viable heart muscle can improve its ability to contract and increase Ejection Fraction.
For severe, end-stage heart failure, advanced measures are considered:
Ventricular Assist Devices (VADs)
A VAD, often an LVAD, is a mechanical pump that takes over the heart’s work. VADs are used temporarily while awaiting a heart transplant (“bridge to transplant”) or as a permanent solution (“destination therapy”).
Heart Transplantation
Heart transplantation remains the final therapy, replacing the failing heart with a healthy donor organ.
Lifestyle Changes Supporting Recovery
Medical treatments are enhanced by consistent lifestyle modifications that reduce daily strain on the heart. Managing fluid and sodium intake is fundamental because excess salt causes water retention, increasing the blood volume the heart must pump. Sodium intake is typically limited to around 2,000 milligrams per day, though this varies by condition severity.
Fluid restriction (often 1.5 to 2 liters daily) is usually reserved for patients with advanced heart failure or those struggling with fluid retention despite medication. Patients should monitor their body weight daily; a rapid gain of two to three pounds over a couple of days indicates fluid accumulation requiring medical attention. Avoiding tobacco and limiting alcohol is also necessary, as both substances directly damage the heart muscle.
Structured, prescribed exercise through cardiac rehabilitation is a highly effective non-pharmacological intervention. This supervised therapy is proven to improve exercise capacity and quality of life for most people with HFrEF. Regular physical activity helps the body use oxygen more efficiently, strengthens muscles, and contributes to reverse remodeling and improved EF.