Does an elderly male with a low stroke volume index (SVI) and normal ejection fraction (EF) have heart failure with preserved ejection fraction (HFpEF) or is he at risk of developing it if compensatory mechanisms fail?

Does This Patient Have HFpEF or Tissue Hypoperfusion?

This patient does not currently meet diagnostic criteria for HFpEF because he lacks symptoms, which are required for the diagnosis, despite having a concerning hemodynamic profile with low stroke volume index. 1

Understanding the Clinical Picture

Current Diagnostic Status

• HFpEF requires both preserved EF (≥50%) AND symptoms (exertional dyspnea, fatigue, or exercise intolerance), according to ACC/AHA guidelines 1

• This patient has:

  • Normal EF of 55-60% (meets the ≥50% threshold) 1
  • Low SVI of 23.69 ml/m² (significantly below normal threshold of >35 ml/m²) 2
  • No reported symptoms or functional limitations (does not meet symptomatic criteria)

• He is currently in a pre-clinical or compensated state where hemodynamic abnormalities exist but have not yet manifested as symptomatic heart failure 1

The Significance of Low Stroke Volume Index

Low SVI is an independent predictor of incident heart failure even with preserved ejection fraction, making this patient at substantial risk for developing symptomatic HFpEF 3

• In the Strong Heart Study, SVI ≤22 ml/m² was associated with 38% higher risk of incident HF (HR 1.38,95% CI 1.06-1.80), independent of EF, LV geometry, and other confounders 3
• Low SVI in patients with preserved EF predicts future HF development over a mean 12-year follow-up 3
• In patients with AF and HFpEF, low SVI (≤35 ml/m²) was associated with significantly worse prognosis, with only 58% event-free survival at mean follow-up 2

Is He Suffering from Tissue Hypoperfusion?

Likely not clinically significant hypoperfusion at rest, given his asymptomatic status and ability to perform daily activities without limitation 1

However, important caveats exist:

• Compensatory mechanisms are currently maintaining adequate perfusion at rest and with usual activities 1

• His low SVI suggests reduced cardiac reserve capacity that may become inadequate with:

  • Increased metabolic demands (exercise, stress, illness) 1
  • Acute decompensation triggers (infection, arrhythmia, dietary indiscretion) 4
  • Progressive deterioration of cardiac function 3

• Subclinical organ hypoperfusion during exertion cannot be excluded without formal exercise testing 5

Risk Stratification and Future Trajectory

High-Risk Features Present

This patient demonstrates several concerning markers:

• Elderly age (70 years) - HFpEF prevalence increases with aging 1
• Low SVI (23.69 ml/m²) - well below the 35 ml/m² threshold associated with adverse outcomes 3, 2
• Male gender - though women are disproportionately affected by HFpEF, men with low SVI have higher risk 3

Likely Trajectory if Compensatory Mechanisms Fail

If compensatory mechanisms fail, he will likely develop symptomatic HFpEF rather than HFrEF, given his currently preserved ejection fraction 1

The progression pathway typically involves:

1. Current state: Asymptomatic with hemodynamic abnormalities (low SVI, preserved EF)
2. Decompensation triggers: Hypertension, atrial fibrillation, obesity, diabetes, coronary disease, or renal dysfunction 1
3. Symptomatic HFpEF: Exercise intolerance, dyspnea, fatigue with preserved EF ≥50% 1
4. Potential complications: Frequent hospitalizations, loss of functional independence, increased mortality 1

Common Precipitants to Monitor

Identify and aggressively manage these common HFpEF risk factors 1:

• Hypertension - present in >80% of HFpEF patients and major risk factor 1
• Obesity/metabolic syndrome - present in >80% of HFpEF cases 1
• Diabetes - affects 25-50% of HFpEF patients with adverse prognostic significance 1
• Atrial fibrillation - can precipitate acute decompensation and further reduce SVI 4, 2
• Coronary artery disease - associated with worse outcomes in HFpEF 1
• Renal dysfunction - bidirectional relationship with heart failure 1

Clinical Recommendations

Immediate Evaluation Needed

Perform comprehensive assessment to identify underlying causes and risk factors 1, 5:

• Screen for hypertension, diabetes, obesity, coronary disease, and renal dysfunction 1
• Evaluate for atrial fibrillation (which can significantly reduce SVI despite preserved EF) 2
• Consider BNP/NT-proBNP measurement (elevated levels predict HF risk even when asymptomatic) 1
• Invasive hemodynamic assessment with exercise provocation may be warranted to definitively assess for incipient HFpEF if clinical suspicion remains high 5

Preventive Strategy

Aggressive risk factor modification is critical to prevent progression to symptomatic HFpEF 1:

• Optimize blood pressure control (though less effective once HFpEF established) 1
• Address obesity through weight loss and metabolic management 1
• Implement supervised exercise training program to improve cardiorespiratory fitness 1
• Manage diabetes aggressively if present 1
• Consider SGLT2 inhibitors for long-term prevention given emerging evidence 4

Monitoring Plan

Serial echocardiography and clinical assessment every 6-12 months to detect:

• Development of symptoms (dyspnea, fatigue, exercise intolerance) 1
• Changes in SVI or diastolic function parameters 1
• Decline in EF (though may remain preserved even with symptomatic progression) 1
• Emergence of comorbidities that increase HFpEF risk 1

Critical Pitfalls to Avoid

• Do not dismiss low SVI as clinically insignificant simply because the patient is asymptomatic - it predicts future HF development 3
• Do not wait for symptoms to develop before implementing preventive strategies - early intervention on risk factors is crucial 1
• Do not assume adequate tissue perfusion based solely on normal resting cardiac output - exercise capacity and reserve may be significantly impaired 5
• Do not overlook atrial fibrillation, which can dramatically reduce SVI despite preserved EF and precipitate decompensation 2