Chronic heart failure is a complex condition where the heart struggles to pump enough blood to meet the body’s demands. This inadequacy can affect various body functions, leading to a range of symptoms. Heart failure can present differently depending on how the heart’s pumping ability is affected, making it important to understand these distinctions.
Understanding Preserved Ejection Fraction
Ejection fraction (EF) measures the percentage of blood pumped out of the heart’s main pumping chamber, the left ventricle, with each beat. A healthy heart typically ejects between 50% and 70% of the blood within its left ventricle during contraction.
In chronic heart failure with preserved ejection fraction (HFpEF), this percentage remains normal or “preserved,” usually at 50% or higher. The apparent paradox arises because despite a normal pumping percentage, the heart still cannot deliver sufficient blood. This occurs because the left ventricle becomes stiff and less able to relax properly between beats.
This stiffness, known as diastolic dysfunction, prevents the ventricle from filling adequately with blood in the first place. Imagine a stiff sponge that cannot soak up much water; even if it wrings out a high percentage of the small amount it holds, the total volume released is low. Similarly, a stiff left ventricle fills with less blood, so even a normal ejection percentage results in an insufficient total amount of blood being pumped out to the body. This impaired filling leads to a backup of pressure in the heart and lungs, causing the symptoms associated with heart failure.
Causes and Associated Conditions
The development of ventricular stiffness in HFpEF is often a result of long-term stressors on the heart, rather than a single direct cause. These stressors frequently stem from a complex interplay of chronic medical conditions.
Long-standing high blood pressure, or hypertension, is a highly common contributing factor to HFpEF. Chronic pressure overload forces the left ventricle to work harder, leading to the thickening and stiffening of its muscle, a condition known as concentric left ventricular hypertrophy. This structural change impairs the heart’s ability to relax and fill efficiently.
Diabetes also plays a significant role, affecting a substantial portion of individuals with HFpEF. The metabolic changes associated with diabetes, such as high blood sugar and altered fat metabolism, can trigger systemic inflammation and endothelial dysfunction. These processes contribute to the formation of advanced glycation end products and fibrosis, directly increasing the stiffness of the left ventricle.
Obesity is another prevalent risk factor, impacting a large majority of HFpEF patients. Excess weight contributes through multiple pathways, including increased blood volume, which puts more strain on the heart, and chronic low-grade inflammation. This inflammation can lead to microvascular damage and fibrosis within the heart muscle, further exacerbating its stiffness and impaired relaxation.
Coronary artery disease, while more commonly associated with heart failure where the pumping ability is reduced, is also frequently found in HFpEF. It can contribute to diastolic dysfunction by causing myocardial ischemia, or reduced blood flow to the heart muscle, leading to stiffness and scarring over time.
Atrial fibrillation, an irregular and often rapid heart rhythm, is highly common among those with HFpEF. These two conditions often coexist due to shared underlying risk factors like systemic inflammation and structural heart changes. Atrial fibrillation can further impair the heart’s ability to fill properly by disrupting the coordinated contraction of the atria, which normally assists in ventricular filling.
The Diagnostic Process
Diagnosing chronic heart failure with preserved ejection fraction often begins when individuals experience symptoms like shortness of breath, particularly during exertion, or persistent fatigue. Swelling in the legs or abdomen, and difficulty breathing when lying flat, are also common indicators. However, these symptoms can overlap with other conditions, making a precise diagnosis challenging.
An echocardiogram is a primary diagnostic tool. This ultrasound of the heart provides detailed images of its structure and function, allowing doctors to measure the ejection fraction and assess the left ventricle’s relaxation and filling properties. It can reveal abnormalities such as increased ventricular wall thickness, left atrial enlargement, and elevated filling pressures, even if the heart’s pumping percentage is within the normal range.
Blood tests are also an important part of the diagnostic process, measuring natriuretic peptides like B-type natriuretic peptide (BNP) or N-terminal pro-B-type natriuretic peptide (NT-proBNP). These substances are released when the heart muscle is stretched or stressed, and elevated levels can suggest heart failure. However, in some HFpEF patients, especially those with obesity, these levels might be lower than expected despite elevated heart pressures, requiring careful interpretation.
An electrocardiogram (ECG) records the heart’s electrical activity and can provide clues about underlying heart conditions. While an ECG may show signs of left ventricular hypertrophy or arrhythmias like atrial fibrillation, there are no specific ECG patterns that definitively diagnose HFpEF on their own. Its role is often supportive.
In some cases, when non-invasive tests are inconclusive, cardiac catheterization may be performed. This invasive procedure involves inserting a thin tube into a blood vessel to directly measure pressures within the heart chambers and pulmonary arteries. Exercise cardiac catheterization, where pressures are measured both at rest and during physical activity, is considered the most accurate method to confirm elevated filling pressures characteristic of HFpEF.
Management and Treatment Strategies
Managing chronic heart failure with preserved ejection fraction involves a multi-faceted approach focused on relieving symptoms, improving quality of life, and addressing the underlying conditions that contribute to the heart’s stiffness.
Lifestyle modifications form a foundational part of the management plan. Restricting sodium intake, often to less than 2 to 3 grams daily, and managing fluid consumption can significantly reduce fluid buildup and alleviate symptoms like swelling and shortness of breath. Regular physical activity, tailored to an individual’s capabilities, can improve exercise tolerance, help relax the heart muscle, and support overall cardiovascular health.
Maintaining a healthy weight is particularly beneficial, as excess body fat increases the heart’s workload and can worsen symptoms. Weight loss programs, combining dietary changes and increased physical activity, can lead to improvements in heart structure and function. Quitting smoking is also highly recommended to prevent further damage to the cardiovascular system.
Medical treatments are prescribed to manage symptoms and address the heart’s underlying issues. Diuretics, such as furosemide or torsemide, are commonly used to reduce fluid overload and alleviate congestion. These medications help the body eliminate excess water and salt, improving breathing and reducing swelling.
Controlling blood pressure and heart rate is also a primary focus. Medications like ACE inhibitors or angiotensin receptor blockers are often prescribed to manage high blood pressure, aiming for a target often below 130/80 mmHg. Beta-blockers may be used to control heart rate, especially in patients with co-existing atrial fibrillation, which can help improve the heart’s filling time.
Newer therapies, such as sodium-glucose cotransporter-2 (SGLT2) inhibitors, have shown significant promise in improving outcomes for individuals with HFpEF. Medications like empagliflozin and dapagliflozin have been shown to reduce hospitalizations for heart failure and cardiovascular death, regardless of whether a person has diabetes. Mineralocorticoid receptor antagonists, like spironolactone, may also be beneficial for some patients with persistent symptoms and elevated natriuretic peptide levels.