How can favorable nuclear test results be reconciled with a low Stroke Volume Index (SVI), declining Left Ventricular Ejection Fraction (LVEF), Chronic Kidney Disease (CKD) stage 3a, and signs of decompensation, including bilateral mild pitting edema and probable Heart Failure with preserved Ejection Fraction (HFpEF)?

Reconciling Favorable Nuclear Test Results with Low SVI and Clinical Decompensation

The favorable nuclear test comments likely reflect preserved global left ventricular ejection fraction and absence of significant ischemia or large perfusion defects, but nuclear imaging has critical limitations in detecting the specific pathophysiology of HFpEF—it does not assess diastolic dysfunction, elevated filling pressures, or the stroke volume index that are central to your patient's decompensation. 1

Understanding the Apparent Discordance

What Nuclear Testing Actually Measures

• Nuclear myocardial perfusion imaging (MPI) primarily evaluates myocardial ischemia, infarction, and global LVEF—it does not directly assess diastolic function, filling pressures, or stroke volume index that are critical in HFpEF. 1

• Resting nuclear ventriculography can evaluate LVEF and ventricular volumes but provides limited information about the hemodynamic derangements characteristic of HFpEF, such as elevated left ventricular end-diastolic pressure or impaired ventricular-arterial coupling. 1

• Comments like "excellent heart function" from nuclear studies typically refer to preserved LVEF (55-60% in your patient) and absence of large perfusion defects—this does not exclude HFpEF, which by definition occurs with preserved or mildly reduced ejection fraction. 1

Why HFpEF Can Coexist with "Normal" Nuclear Results

• HFpEF is fundamentally a disorder of diastolic dysfunction, elevated filling pressures, and impaired cardiac reserve—not primarily a disorder of systolic ejection fraction or myocardial perfusion. 1, 2

• Your patient's LVEF of 55-60% falls within the HFpEF range (≥50%), so preserved ejection fraction on nuclear imaging is entirely consistent with—not contradictory to—HFpEF diagnosis. 1, 2

• The critical abnormality is the severely reduced stroke volume index (SVI 23.69 mL/m²)—normal SVI is typically 35-65 mL/m², indicating your patient is ejecting a small absolute volume despite preserved ejection fraction percentage. 2, 3

The Clinical Picture Supports HFpEF with Cardiorenal Syndrome

Evidence of Decompensation

• Bilateral mild pitting edema of both ankles represents objective evidence of systemic congestion, which is a cardinal feature of decompensated heart failure and supports the HFpEF diagnosis regardless of nuclear test results. 1, 2

• The combination of symptoms/signs of heart failure, preserved LVEF (55-60%), and evidence of congestion fulfills diagnostic criteria for HFpEF, even without elevated natriuretic peptides if other cardiac structural/functional abnormalities are present. 1, 2

The Declining LVEF Trajectory is Concerning

• The decline from 65-70% to 55-60% represents a meaningful reduction in systolic function over time, suggesting progressive myocardial dysfunction despite remaining in the "preserved" EF range. 1, 3

• This trajectory warrants urgent specialist evaluation as recommended by guidelines for patients with changing clinical status or worsening heart failure symptoms. 1

Cardiorenal Syndrome Explains Much of the Clinical Picture

• CKD stage 3a (eGFR 58.5, creatinine 130 μmol/L) with declining renal function is extremely common in HFpEF and represents cardiorenal syndrome type 2 (chronic heart failure leading to progressive CKD). 4, 5, 6

• CKD is independently associated with worse cardiac mechanics in HFpEF, including reduced left atrial reservoir strain and left ventricular longitudinal strain—abnormalities that nuclear imaging does not detect. 5

• The bidirectional relationship between heart and kidney dysfunction creates a vicious cycle: fluid retention from renal dysfunction worsens cardiac filling pressures, while reduced cardiac output and venous congestion further impair renal perfusion. 4, 7

• Renal dysfunction is a stronger predictor of adverse outcomes in heart failure patients, and the steady decline in eGFR indicates progressive cardiorenal syndrome requiring specialist management. 5, 6

Why Nuclear Imaging Misses HFpEF Pathophysiology

Limitations of Nuclear Cardiology in HFpEF

• Nuclear imaging provides limited information about diastolic dysfunction, which is the fundamental abnormality in HFpEF—it cannot assess E/e' ratios, left atrial enlargement, or elevated filling pressures. 1

• Chest radiography and nuclear ventriculography are insensitive for monitoring heart failure and detecting changes in hemodynamic status compared to echocardiography or invasive hemodynamic assessment. 1

• The ACR Appropriateness Criteria note limited evidence for nuclear imaging as follow-up in known heart failure, emphasizing that echocardiography remains the primary modality for assessing cardiac structure and function. 1

What Testing Would Better Assess This Patient

• Transthoracic echocardiography with comprehensive diastolic assessment (E/A ratio, E/e' ratio, left atrial volume index, tricuspid regurgitation velocity) is essential for diagnosing HFpEF and should be performed or repeated. 1, 2

• Natriuretic peptide measurement (BNP >35 pg/mL or NT-proBNP >125 pg/mL in ambulatory setting) supports HFpEF diagnosis, though levels may be lower in obesity and do not exclude HFpEF if clinical and imaging criteria are met. 1, 2

• If diagnosis remains uncertain after echocardiography, invasive hemodynamic assessment or exercise stress testing may be needed to confirm elevated filling pressures characteristic of HFpEF. 1, 2

Clinical Implications and Urgent Actions

The Heart Failure Specialist Referral is Appropriate

• Your patient meets multiple high-risk criteria warranting specialist evaluation: severely reduced SVI, declining LVEF trajectory, CKD stage 3a with declining eGFR, and clinical decompensation with edema. 1

• The European Society of Cardiology recommends reassessment by specialists for patients with worsening heart failure symptoms or important cardiovascular events, which applies to your patient's decompensation. 1

Management Priorities Pending Specialist Evaluation

• Optimize volume status with diuretics to address the bilateral pitting edema and systemic congestion, which is fundamental to HFpEF management. 1

• Consider renin-angiotensin system inhibitors if not already prescribed, as they are associated with reduced adverse cardiovascular outcomes in HFpEF patients with mild to moderate CKD. 8

• Monitor renal function closely during diuresis given the cardiorenal syndrome—creatinine may rise transiently with decongestion but should stabilize. 4, 6

• Avoid over-reliance on the "favorable" nuclear test results when making clinical decisions—the patient's symptoms, signs, hemodynamics (low SVI), and declining renal function are more relevant to current management than perfusion imaging. 1, 2

Key Pitfall to Avoid

The most critical error would be false reassurance from "excellent" nuclear test comments leading to delayed specialist referral or inadequate treatment of decompensated HFpEF—nuclear imaging excellence refers to perfusion and global EF, not the diastolic dysfunction, low stroke volume, and elevated filling pressures that define your patient's syndrome. 1, 2