How do the clinical presentations of systolic heart failure (heart failure with reduced ejection fraction) differ from diastolic heart failure (heart failure with preserved ejection fraction)?

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Clinical Presentation: Systolic vs Diastolic Heart Failure

Critical First Point: Symptoms Are Identical

You cannot distinguish systolic heart failure (HFrEF) from diastolic heart failure (HFpEF) based on clinical presentation alone—both conditions produce identical symptoms and signs of heart failure, and echocardiography is mandatory to differentiate them. 1, 2

Shared Clinical Features (Indistinguishable by Examination)

Both HFrEF and HFpEF present with:

  • Dyspnea (exertional or at rest), fatigue, and ankle swelling as the cardinal symptoms 3, 1
  • Elevated jugular venous pressure, pulmonary crackles, and peripheral edema on physical examination 2
  • Similar neurohormonal activation (renin-angiotensin-aldosterone system, sympathetic nervous system) despite different underlying mechanisms 1
  • Comparable exercise intolerance and reduced functional capacity 4
  • Equivalent severity of diastolic filling abnormalities—regardless of ejection fraction, the degree of diastolic dysfunction correlates with symptom severity and prognosis 4

Key Pathophysiologic Differences (Not Clinically Apparent)

Systolic Heart Failure (HFrEF, LVEF ≤40%)

  • Impaired forward pump function is the primary defect—the heart cannot generate adequate cardiac output, triggering compensatory neurohormonal activation 1
  • Ventricular dilation with large end-diastolic volumes and elongated myocytes characterize the remodeling pattern 1, 2, 4
  • Reduced contractility makes positive inotropic agents potentially beneficial 1
  • Most commonly caused by ischemic heart disease or dilated cardiomyopathy 2

Diastolic Heart Failure (HFpEF, LVEF ≥50%)

  • Impaired ventricular filling is the core problem—diminished relaxation during early diastole and reduced compliance cause a stiff ventricle 1
  • Elevated filling pressures drive pulmonary congestion despite preserved systolic pump function 1
  • Stroke volume and cardiac output remain normal at rest due to compensatory high filling pressures, but become compromised during exercise 1
  • Increased wall thickness, left atrial enlargement, and normal or minimally enlarged ventricular cavity define the structural phenotype 2, 5
  • Combined ventricular-systolic and arterial stiffening amplifies blood pressure lability and worsens diastolic dysfunction under stress 6
  • Positive inotropic agents are not useful because systolic function is preserved 1

Demographic and Comorbidity Patterns (Provide Clinical Clues)

HFpEF Patient Profile

  • Predominantly elderly women with hypertension—HFpEF accounts for 20–60% of all heart failure cases and is more prevalent in females 1, 7, 8
  • High burden of cardiometabolic comorbidities: obesity (BMI >30 kg/m²), diabetes mellitus, chronic kidney disease, and atrial fibrillation occur disproportionately 2, 7, 5
  • History of pre-eclampsia increases subsequent HFpEF risk in women 7

HFrEF Patient Profile

  • More common in men and younger patients relative to HFpEF 7
  • Ischemic heart disease is the leading etiology 2

Prognostic Differences

  • HFpEF carries lower annual mortality (approximately 8%) compared to HFrEF (19%), but morbidity remains substantial and hospitalization rates are equivalent 1
  • Both conditions share similar 90-day mortality and readmission rates 9

Diagnostic Algorithm (Mandatory Steps)

  1. Obtain transthoracic echocardiography first to measure LVEF—this single test categorizes the phenotype (HFrEF ≤40%, HFmrEF 41–49%, HFpEF ≥50%) and directs all subsequent therapy 2

  2. Measure BNP or NT-proBNP to confirm the diagnosis and stratify prognosis—markedly elevated values provide diagnostic certainty 2

  3. For HFpEF, require objective evidence of elevated filling pressures: elevated natriuretic peptides and/or echocardiographic diastolic parameters (E/e′ ≥15) and/or invasive hemodynamic confirmation 1, 2

  4. Assess for structural abnormalities: HFpEF patients typically show increased wall thickness and left atrial enlargement without ventricular dilation 2, 5

Therapeutic Implications (Fundamentally Different)

HFrEF (Evidence-Based Mortality Reduction)

  • Four-pillar guideline-directed medical therapy (GDMT) reduces mortality: ARNI (sacubitril/valsartan), beta-blockers, mineralocorticoid receptor antagonists, and SGLT2 inhibitors 2, 7
  • ACE inhibitors are first-line if ARNI is unavailable 1, 2
  • Diuretics manage volume overload 1
  • Device therapy (ICD, CRT) improves outcomes in selected patients with LVEF ≤35% 2, 7

HFpEF (Symptom Control and Comorbidity Management)

  • No therapies that reduce mortality in HFrEF have shown similar benefit in HFpEF—management focuses on symptom relief and comorbidity optimization 1, 7
  • SGLT2 inhibitors (dapagliflozin 10 mg or empagliflozin 10 mg daily) reduce the composite endpoint of cardiovascular death and HF hospitalizations by 18–21% 7
  • Diuretics and nitrates reduce elevated filling pressures, but must be started at small doses with careful monitoring to prevent hypotension—the goal is to lower filling pressures without reducing cardiac output 1
  • Beta-blockers or calcium channel blockers improve diastolic filling by reducing heart rate and allowing more time for ventricular filling 1
  • Aggressive blood pressure control targeting <130/80 mmHg is paramount 1, 7
  • Exercise training (Class I recommendation) produces large, clinically meaningful improvements in exercise capacity and quality of life 7, 9
  • Weight reduction in obese patients addresses a major contributor to HFpEF pathophysiology 7
  • Rate control is essential if atrial fibrillation develops, using agents that suppress AV conduction 1

Common Pitfalls to Avoid

  • Never rely on symptoms, signs, or natriuretic peptide levels alone to distinguish HFrEF from HFpEF—echocardiography is non-negotiable 1, 2
  • Do not assume "diastolic heart failure" means only diastolic dysfunction—most HFrEF patients also have diastolic abnormalities at rest, and many HFpEF patients have subtle contractile abnormalities despite preserved ejection fraction 3, 4
  • Abandon outdated terminology ("systolic heart failure," "diastolic heart failure," "congestive heart failure")—use LVEF-based classification (HFrEF, HFmrEF, HFpEF) to avoid oversimplification and potential mistreatment 1, 2
  • Do not extrapolate HFrEF therapies to HFpEF—positive inotropes are contraindicated in HFpEF, and neurohormonal antagonists lack proven mortality benefit 1, 7
  • In HFpEF, avoid aggressive diuresis—excessive preload reduction can precipitate hypotension and reduce cardiac output because these patients depend on elevated filling pressures to maintain stroke volume 1

References

1
Guideline

Heart Failure Management and Pathophysiology

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2026

2
Guideline

Evidence‑Based Diagnosis and Management of Heart Failure by Ejection‑Fraction

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2026

3
Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

7
Guideline

Management of Heart Failure with Reduced and Preserved Ejection Fraction

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2026

9
Research

Heart Failure With Preserved Ejection Fraction.

The Journal of the American Osteopathic Association, 2015

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Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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