For individuals managing heart conditions, the Ejection Fraction (EF) is a fundamental metric for evaluating the heart’s pumping efficiency. When the heart muscle weakens, its ability to propel blood into circulation declines, a condition often associated with heart failure. Improving a low EF is a primary goal in management, aiming for better quality of life and increased longevity. Management involves a tiered approach, starting with medical therapy and lifestyle changes before considering advanced procedural options.
Understanding Ejection Fraction
Ejection Fraction (EF) is a percentage measurement representing how much blood the left ventricle pumps out with each contraction. It is the percentage of blood volume ejected compared to the total volume available at the end of the filling phase. This measurement, usually focused on the left ventricle (LVEF), is the most common way physicians assess the heart’s systolic function.
The most common method for measuring EF is an echocardiogram, a non-invasive test using sound waves to create moving images of the heart. Other advanced techniques like cardiac MRI are sometimes used for precise volume calculations. A normal EF falls between 50% and 70%, indicating effective pumping action.
When the EF drops to 40% or lower, it is classified as heart failure with reduced ejection fraction (HFrEF), or systolic heart failure. An EF between 41% and 49% is considered mildly reduced. A low EF signals maladaptive cardiac remodeling, where the ventricle enlarges and changes shape, reducing its pumping power. Therapeutic intervention aims to halt or reverse this remodeling and restore mechanical efficiency.
Pharmacological Strategies
Medications are the foundational treatment for increasing a reduced EF, counteracting the pathological processes that cause the heart to weaken. A combination of four distinct drug classes is the standard of care to maximize cardiac reverse remodeling and improve patient outcomes. These therapies work synergistically to block the harmful effects of the body’s overactive stress hormones, which contribute to heart enlargement and fibrosis.
One cornerstone therapy involves Angiotensin Receptor-Neprilysin Inhibitors (ARNIs), such as sacubitril/valsartan, often favored over older ACE inhibitors or ARBs. ARNIs block the harmful effects of the renin-angiotensin system while preventing the breakdown of natural vasodilating peptides. Enhancing these natriuretic peptides promotes vasodilation and fluid excretion, reducing cardiac strain. This significantly promotes left ventricular reverse remodeling, leading to an increase in EF.
Beta-blockers, such as carvedilol or metoprolol succinate, counteract the chronic over-stimulation of the sympathetic nervous system. This class of drugs reduces the heart rate and lessens the cardiotoxic effects of stress hormones like adrenaline. This allows the heart to relax and fill more completely. This sustained reduction in strain helps the heart muscle recover over time, leading to a measurable increase in LVEF.
Mineralocorticoid Receptor Antagonists (MRAs), including spironolactone and eplerenone, target the effects of the hormone aldosterone. Aldosterone contributes to sodium retention and causes fibrosis and scarring in the heart muscle. By blocking this receptor, MRAs reduce fluid retention and mitigate pathological scarring, supporting reverse remodeling and improved cardiac function.
The newest addition to the core treatment strategy is the class of Sodium-Glucose Cotransporter 2 (SGLT2) Inhibitors. Initially developed for diabetes, they benefit heart failure patients regardless of blood sugar status. These drugs, like dapagliflozin and empagliflozin, exert beneficial effects through mild diuresis and natriuresis, reducing the heart’s workload. They also appear to improve the heart muscle’s energy metabolism, leading to an improvement in EF and a reduction in hospitalizations.
Essential Lifestyle Modifications
While medications work at a cellular level, essential lifestyle adjustments complement therapy by reducing the daily workload on the heart. Managing fluid balance is paramount, achieved through careful control of dietary sodium and daily fluid intake. Physicians often recommend limiting sodium intake to less than 2,000 milligrams per day to prevent excess water retention. For patients with advanced heart failure, fluid intake may need to be restricted to 1.5 to 2 liters daily, which directly reduces volume overload.
Daily weight monitoring provides an early warning sign of fluid retention. Patients should weigh themselves every morning. A sudden weight gain (3 pounds in 2 to 3 days or 5 pounds in a week) should prompt immediate contact with a healthcare provider. This intervention allows for a simple adjustment of diuretic medication to eliminate excess fluid, preventing hospitalization.
Structured exercise, often delivered through a formal cardiac rehabilitation program, is a highly recommended component of self-management. Regular, tailored physical activity has been shown to improve exercise capacity, quality of life, and directly contributes to left ventricular reverse remodeling. Exercise causes favorable changes in the skeletal muscles and improves the heart’s ability to pump blood, even in those with a significantly reduced EF.
Finally, eliminating harmful substances is non-negotiable for anyone seeking to improve their EF. Smoking cessation is one of the most impactful changes, as current smokers have a significantly elevated risk of heart failure compared to non-smokers. Excessive alcohol consumption can directly damage the heart muscle, and abstinence can often lead to a measurable recovery of the left ventricular ejection fraction.
Device and Surgical Options
For patients whose EF remains low despite optimized medical therapy and rigorous lifestyle changes, advanced interventions become necessary. Implantable Cardioverter-Defibrillators (ICDs) are electronic devices placed in the chest to monitor heart rhythm. While an ICD does not directly increase the ejection fraction, it is a life-saving measure indicated for primary prevention of sudden cardiac death in patients with an LVEF of 35% or less. The device delivers a shock to restore a normal rhythm if a dangerous, rapid heart rhythm is detected.
Cardiac Resynchronization Therapy (CRT), which involves a specialized pacemaker, is another procedural option designed to improve the heart’s mechanical efficiency. This therapy, also known as biventricular pacing, is used when the left and right ventricles contract out of sync, a problem common in HFrEF. By placing leads in both ventricles to coordinate their contraction, CRT restores synchrony and can lead to a significant increase in EF, often by 4% to over 10%, which promotes reverse remodeling.
For individuals with end-stage heart failure that is unresponsive to all other treatments, more drastic interventions are considered. A Ventricular Assist Device (VAD) is a mechanical pump implanted into the chest that helps the weakened ventricle circulate blood throughout the body. VADs can serve as a bridge to heart transplantation or as destination therapy for those not eligible for a transplant. Ultimately, orthotopic heart transplantation remains the only truly curative option for end-stage heart failure, replacing the diseased heart entirely.