Introduction
Heart failure (HF) is a complex clinical syndrome characterized by the heart’s inability to pump blood effectively to meet the body’s metabolic demands. It represents a final common pathway of various cardiovascular diseases including coronary artery disease (CAD), hypertension, valvular disorders, and cardiomyopathies. Traditionally, heart failure was regarded as a single entity, but advances in diagnostic imaging—particularly echocardiography—have allowed clinicians to recognize two major phenotypes:
- Systolic Heart Failure → also called Heart Failure with Reduced Ejection Fraction (HFrEF)
- Diastolic Heart Failure → also called Heart Failure with Preserved Ejection Fraction (HFpEF)
These classifications are not merely academic distinctions—they reflect different pathophysiological mechanisms, therapeutic strategies, and prognoses.
This article explores the differences between systolic and diastolic heart failure in detail, covering definitions, underlying mechanisms, clinical presentations, and outcomes.
Definitions: HFrEF vs. HFpEF
1. Systolic Heart Failure (HFrEF)
- Defined as heart failure with a reduced left ventricular ejection fraction (LVEF).
- LVEF < 40% is the most widely accepted cutoff.
- The hallmark problem is impaired contractility of the left ventricle, leading to reduced stroke volume and cardiac output.
- Common causes: ischemic cardiomyopathy, dilated cardiomyopathy, myocarditis, chronic pressure overload.
2. Diastolic Heart Failure (HFpEF)
- Defined as heart failure with preserved ejection fraction, usually LVEF ≥ 50%.
- The primary abnormality lies in diastolic dysfunction—the left ventricle fails to relax and fill properly during diastole.
- Stroke volume is reduced despite preserved EF because of stiff ventricular walls and impaired compliance.
- Common causes: chronic hypertension, hypertrophic cardiomyopathy, aging, obesity, diabetes.
3. The “Mid-range” Phenotype (HFmrEF)
- An intermediate group, LVEF 41–49%, sometimes overlaps between systolic and diastolic HF.
- Research is ongoing to determine whether HFmrEF behaves more like HFrEF or HFpEF.
Key takeaway:
- HFrEF = weak pump (problem with contraction).
- HFpEF = stiff pump (problem with relaxation).
Pathophysiological Differences
Although both phenotypes lead to similar symptoms (dyspnea, fatigue, fluid retention), their pathophysiology diverges significantly.
1. Systolic Heart Failure (HFrEF) Pathophysiology
- Impaired Contractility:
- Loss of viable myocardium (e.g., after MI) or dilated cardiomyopathy reduces the force of contraction.
- Stroke volume and cardiac output drop.
- Neurohormonal Activation:
- Decreased cardiac output activates sympathetic nervous system (SNS) and renin-angiotensin-aldosterone system (RAAS).
- Chronic neurohormonal activation leads to vasoconstriction, sodium retention, and progressive ventricular remodeling.
- Ventricular Remodeling:
- LV dilates, walls become thin, and spherical remodeling occurs.
- This worsens contractile dysfunction and increases wall stress.
- Hemodynamic Profile:
- Reduced ejection fraction, high end-systolic volume, elevated left ventricular end-diastolic pressure (LVEDP).
- Pulmonary congestion from backward failure.
2. Diastolic Heart Failure (HFpEF) Pathophysiology
- Impaired Relaxation:
- The left ventricle is stiff and non-compliant, making diastolic filling difficult.
- Even small increases in volume result in significant increases in filling pressure.
- Concentric Remodeling:
- Hypertension-induced hypertrophy thickens LV walls without dilation.
- The cavity size is often normal or reduced.
- Ventricular-Vascular Coupling:
- Increased arterial stiffness (common in elderly, hypertensives, diabetics) exacerbates diastolic dysfunction.
- Microvascular Dysfunction:
- Coronary microvascular inflammation and endothelial dysfunction impair relaxation and filling.
- Hemodynamic Profile:
- Normal EF but reduced stroke volume due to impaired preload.
- Elevated left atrial and pulmonary venous pressures → pulmonary congestion.
3. Key Contrasts
| Feature | HFrEF (Systolic HF) | HFpEF (Diastolic HF) |
|---|---|---|
| LVEF | < 40% | ≥ 50% |
| LV Geometry | Dilated, thin-walled | Thick, stiff walls |
| Pathology | Impaired contraction | Impaired relaxation |
| Stroke Volume | Reduced | Reduced |
| LVEDP | Increased | Increased |
| Remodeling | Eccentric | Concentric |
| Typical Patient | Younger, post-MI, dilated cardiomyopathy | Older, hypertensive, diabetic, obese, women more common |
Clinical Features
Despite their differences, HFrEF and HFpEF share many overlapping symptoms since both lead to congestion and inadequate cardiac output.
1. Shared Symptoms (Both Types)
- Dyspnea on exertion (most common presenting symptom).
- Paroxysmal nocturnal dyspnea (PND) and orthopnea due to pulmonary venous congestion.
- Fatigue and exercise intolerance from low cardiac output.
- Peripheral edema, ascites, hepatomegaly from right-sided involvement.
- Weight gain due to fluid retention.
2. Physical Examination Findings
- Elevated jugular venous pressure (JVP).
- Pulmonary rales or crackles.
- S3 heart sound (common in HFrEF, indicates volume overload).
- S4 heart sound (common in HFpEF, indicates stiff ventricle).
- Displaced apical impulse (HFrEF).
- Sustained apical impulse (HFpEF).
3. Distinguishing Features in Clinical Profile
| Feature | HFrEF | HFpEF |
|---|---|---|
| Age | Younger to middle-aged | Older (>65 years) |
| Gender | More common in men | More common in women |
| Comorbidities | CAD, dilated cardiomyopathy | Hypertension, diabetes, obesity, atrial fibrillation |
| Symptoms onset | May follow MI or myocarditis | Insidious, chronic hypertension |
| Murmurs | MR from dilation | May have AS/HTN-related murmurs |
Outcomes and Prognosis
1. Mortality and Morbidity
- HFrEF:
- Historically associated with high mortality.
- Advances in guideline-directed medical therapy (GDMT)—including beta-blockers, ACE inhibitors, ARBs, ARNIs, mineralocorticoid receptor antagonists (MRAs), and SGLT2 inhibitors—have significantly improved survival.
- 5-year survival remains ~50% in severe cases.
- HFpEF:
- Mortality rates are similar to HFrEF but hospitalization rates are often higher.
- Fewer proven therapies reduce mortality in HFpEF, making it a therapeutic challenge.
- Prognosis worsens with comorbidities (HTN, diabetes, obesity).
2. Hospitalizations
- HFpEF patients are more likely to be elderly with multiple comorbidities → repeated hospitalizations.
- HFrEF hospitalizations are more often due to acute decompensation from poor medication adherence or progression of disease.
3. Response to Therapy
- HFrEF: Robust evidence supports therapies that reduce mortality (e.g., beta-blockers, ACEIs, ARNIs, MRAs, SGLT2 inhibitors).
- HFpEF: Treatment is largely symptomatic, focusing on diuretics for congestion, blood pressure control, and risk factor modification. Recent trials suggest SGLT2 inhibitors may improve outcomes.
4. Quality of Life
- Both types lead to exercise intolerance and impaired daily function.
- HFpEF patients often have a higher symptom burden despite preserved EF.
Diagnostic Considerations
Although your outline didn’t ask for diagnostics, they’re worth mentioning for context:
- Echocardiography:
- Essential for distinguishing HFrEF vs HFpEF (measures EF, LV dimensions, diastolic filling patterns).
- BNP/NT-proBNP: Elevated in both but may be disproportionately higher in HFrEF.
- Cardiac MRI: Can help assess fibrosis and infiltrative diseases (amyloidosis, sarcoidosis).
Summary Table
| Aspect | HFrEF (Systolic HF) | HFpEF (Diastolic HF) |
|---|---|---|
| Definition | LVEF < 40% | LVEF ≥ 50% |
| Pathophysiology | Impaired contractility | Impaired relaxation, stiffness |
| Remodeling | Dilated ventricle | Concentric hypertrophy |
| Common Causes | MI, dilated cardiomyopathy | Hypertension, aging, obesity |
| Symptoms | Dyspnea, fatigue, edema | Same, often more with exertion |
| Prognosis | High mortality, improved with GDMT | Similar mortality, high hospitalization, fewer treatments |
| Treatment | ACEI/ARB/ARNI, beta-blocker, MRA, SGLT2i | Diuretics, BP control, comorbidity management |
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