Heart Failure with Preserved Ejection Fraction
A type of heart failure where the heart pumps normally but is too stiff to relax and fill properly with blood, causing fluid backup into the lungs and body.
Emergency Management: Hypertensive crisis leading to Flash Pulmonary Edema; patients are extremely sensitive to sudden spikes in afterload. Treat with IV Nitroglycerin and non-invasive ventilation.
Heart Failure with Preserved Ejection Fraction (HFpEF) is a clinical syndrome characterized by signs and symptoms of heart failure with normal or near-normal left ventricular systolic function (LVEF ≥ 50%). The primary defect is diastolic dysfunction: the left ventricle becomes stiff, hypertrophied, and non-compliant, impairing its ability to relax and fill adequately at normal filling pressures.
Detailed Overview
HFpEF accounts for approximately half of all heart failure cases and is increasingly recognized as a systemic, proinflammatory, multiorgan syndrome rather than an isolated cardiac disease. It is strongly driven by comorbidities like aging, obesity, hypertension, and metabolic syndrome. The clinical significance of HFpEF is profound due to its soaring prevalence, high morbidity, and historical lack of disease-modifying therapies, though recent trials with SGLT2 inhibitors have marked a breakthrough. The stiffened ventricle requires elevated atrial pressures to fill, leading to backward congestion into the pulmonary and systemic veins.
Epidemiology & Demographics
Prevalence is rising due to an aging population and obesity epidemic. Accounts for >50% of heart failure hospitalizations. Predominantly affects older adults (often >70 years) and has a higher prevalence in females compared to HFrEF.
Etiological Mechanism
The etiology is typically multifactorial, driven by chronic comorbidities that induce systemic microvascular inflammation. Primary drivers are long-standing hypertension (causing LV hypertrophy), obesity, diabetes mellitus, and aging. Infiltrative cardiomyopathies (like Cardiac Amyloidosis) are a distinct, critical etiology within the HFpEF spectrum.
Primary Causes
Chronic hypertension, metabolic syndrome/obesity, normal aging (senile cardiac stiffening), Transthyretin Cardiac Amyloidosis (ATTR), Hypertrophic Cardiomyopathy.
Systemic comorbidities trigger a systemic proinflammatory state, leading to coronary microvascular endothelial inflammation. This reduces nitric oxide (NO) bioavailability, decreasing protein kinase G (PKG) activity in cardiomyocytes. Low PKG causes hypophosphorylation of titin (the giant myocardial spring protein), making the cardiomyocytes excessively stiff. Concurrently, inflammation drives fibroblasts to deposit excess interstitial collagen. The resulting stiff, non-compliant Left Ventricle requires abnormally high Left Atrial (LA) pressures to achieve adequate diastolic filling. This elevated pressure transmits backward, causing pulmonary venous congestion (dyspnea) and right heart failure/systemic congestion (edema), while the inability to augment cardiac output during exercise causes severe fatigue.
Diagnostic Criteria & Guidelines
1. Symptoms/signs of heart failure. 2. LVEF ≥ 50%. 3. Objective evidence of structural heart disease (LV hypertrophy or Left Atrial enlargement) AND/OR diastolic dysfunction (E/e' ratio > 15 on echo). 4. Elevated NT-proBNP (>125 pg/mL, though often lower in obesity). Gold standard is invasive right heart catheterization showing PCWP ≥ 15 mmHg at rest or ≥ 25 mmHg with exercise.
SGLT2 Inhibitors (Empagliflozin 10 mg daily OR Dapagliflozin 10 mg daily) are the FIRST therapies proven to reduce cardiovascular mortality and heart failure hospitalizations in HFpEF. Plus, Loop Diuretics (e.g., Furosemide or Torsemide) PRN to strictly maintain euvolemia and relieve congestion.
Second-Line & Adjunctive Therapy
Mineralocorticoid Receptor Antagonists (Spironolactone 25 mg daily) can decrease hospitalizations, particularly in patients with LVEF on the lower end of normal (50-60%). Strict management of blood pressure and arrhythmias (e.g., rate/rhythm control for AFib) is crucial.
Surgical & Procedural Management
Bariatric surgery for morbidly obese HFpEF phenotypes. Interatrial shunt devices are currently under clinical investigation to decompress the left atrium.
Patient Counseling & Advice
Counsel that while their 'heart squeeze' is normal, their heart is 'stiff.' Emphasize that weight loss and exercise are as important as medications. Managing their other conditions (blood pressure, diabetes) is the key to treating the heart.
Follow-Up & Monitoring Schedule
Regular clinical assessment of volume status (JVP, edema, orthopnea). Monitor renal function and potassium, especially if using Spironolactone or SGLT2i. Echocardiogram to monitor for worsening structural changes.
Preventive Strategies
Preventing the metabolic syndrome: maintaining a normal BMI, regular aerobic exercise, and aggressive control of hypertension and diabetes.
Morbidity is high with frequent readmissions. 5-year mortality approaches 50%, similar to HFrEF, though deaths in HFpEF are more often non-cardiovascular (driven by age and comorbidities). SGLT2 inhibitors are improving this trajectory.