Diastolic Dysfunction, Scoring Systems, and Cardiorenal Connections
Clinical Mastery SeriesUrine Nephrology Now
Andrew Bland, MD, MBA, MS
Current Diagnostic Framework (2022 AHA/ACC/HFSA)
HFpEF diagnosis requires four essential components:
Heart failure symptoms: Exertional dyspnea, fatigue, exercise intolerance, and evidence of congestion
LVEF ≥50% on echocardiography
Evidence of elevated LV filling pressures: Elevated natriuretic peptides, E/e' ≥15, or invasive hemodynamics
Structural heart disease evidence: Increased LA volume index or LV mass index
Clinical Pearl
Women with HFpEF typically exhibit higher EFs due to smaller LV chamber size and more concentric remodeling. An EF of 50–55% may represent abnormal systolic function in women, potentially leading to underdiagnosis with sex-neutral thresholds.
HFimpEF: Patients with previously reduced EF that improved to >40% should continue receiving HFrEF-directed therapy regardless of current EF.
Echocardiographic Diagnostic Criteria
E Wave: Transmitral Early Diastolic Flow Velocity
Peak velocity of early diastolic transmitral flow, measured using pulsed-wave Doppler at mitral valve leaflet tips. Reflects the pressure gradient between LA and LV after mitral valve opening. Normal: 60–100 cm/s in healthy adults (age-dependent).
e' (e-prime): Tissue Doppler Early Diastolic Velocity
Peak early diastolic velocity of the mitral annulus via tissue Doppler. Reflects intrinsic myocardial relaxation properties and is relatively independent of loading conditions.
Septal e': Normal >8 cm/s; impaired <7 cm/s
Lateral e': Normal >10 cm/s; impaired <10 cm/s
E/e' Ratio: The Integrative Measurement
E/e' Value
Interpretation
<8
Normal filling pressures — argues against HFpEF
8–15
Intermediate — requires integration with LAVI, TR velocity, natriuretic peptides
Score ≥5: High likelihood of HFpEF. Score ≤1: HFpEF very unlikely. Score 2–4: Proceed to stress testing.
H2FPEF Score
Component
Criteria
Points
Heavy (BMI)
>30 kg/m²
2
2 antihypertensives
≥2 BP medications
1
Fibrillation
Atrial fibrillation
3
Pulmonary hypertension
PASP >35 mmHg
1
Elder
Age >60
1
Filling pressure
E/e' >9
1
≥6: High probability. <2: Low probability. 2–5: Additional evaluation needed. AUC 0.84 in validation studies.
Approximately 35–45% of patients fall into intermediate probability categories with either scoring system, highlighting continued need for additional testing.
Diastolic Dysfunction vs. HFpEF
Component
Diastolic Dysfunction
HFpEF
Symptoms
Not required; may be asymptomatic
Mandatory
LVEF
≥50%
≥50%
Echo Evidence
Abnormal diastolic parameters sufficient
Requires elevated filling pressures (E/e' ≥15 or additional evidence)
Natriuretic Peptides
Not required; may be normal
Elevated levels support diagnosis
Structural Disease
May be present but not required
Required (LAVI >40 or LVH)
Grading
Grade I (impaired relaxation), II (pseudonormal), III (restrictive)
HFA-PEFF or H2FPEF scoring
Therapy
CV risk factor modification
GDMT: SGLT2i, ARNi/ARB, MRA
Progression
3–5% annual progression to HFpEF
Established diagnosis requiring HF management
HFpEF as a Renal Disease: Emerging Paradigm
CKD prevalence in HFpEF patients approaches 40–50%, significantly higher than age-matched controls. CKD in HFpEF is one of the strongest independent predictors of adverse outcomes.
Pathophysiological Mechanisms
Renal venous congestion: Elevated CVP impairs renal perfusion through increased renal venous pressure and decreased arteriovenous gradient (“kidney tamponade”)
Intra-abdominal pressure: Volume overload causes direct compression of renal parenchyma
Inflammatory pathways: TNF-alpha, IL-6, and CRP directly impair renal endothelial function and promote fibrosis
Metabolic syndrome: Prevalence exceeds 70% in HFpEF; AGEs, oxidative stress, and altered sodium handling contribute
Endothelial dysfunction: Unifying mechanism — reduced NO bioavailability impairs both cardiac relaxation and renal autoregulation
Clinical Pearl
Worsening renal function during effective decongestion therapy requires nuanced interpretation. Acute eGFR decreases may reflect reduced renal venous pressure rather than true kidney injury. Aggressive diuresis often leads to long-term improvement in renal function through reduction of renal congestion.
Future Directions
Novel biomarkers: NGAL and KIM-1 for cardiorenal interactions
Advanced imaging: Cardiac MRI with T1 mapping and renal Doppler ultrasound
Device therapies: Interatrial shunt devices and cardiac contractility modulation
AI applications in echocardiographic interpretation for early detection
Key References
Heidenreich PA, et al. 2022 AHA/ACC/HFSA Guideline for HF Management. Circulation. 2022;145(18):e895–e1032. PubMed
McDonagh TA, et al. 2023 ESC Focused Update. Eur Heart J. 2023;44(37):3627–3639. PubMed
Pieske B, et al. HFA-PEFF diagnostic algorithm. Eur Heart J. 2019;40(40):3297–3317. PubMed
Reddy YNV, et al. H2FPEF Score. Circulation. 2018;138(9):861–870. PubMed
Borlaug BA, et al. HFpEF: JACC Scientific Statement. J Am Coll Cardiol. 2023;81(18):1810–1834. PubMed
Nagueh SF, et al. ASE 2025 Recommendations for LV Diastolic Function. J Am Soc Echocardiogr. 2025;38(7):537–569. PubMed Search
Solomon SD, et al. Dapagliflozin in HFmrEF/HFpEF (DELIVER). N Engl J Med. 2022;387(12):1089–1098. PubMed
Anker SD, et al. Empagliflozin in HFpEF (EMPEROR-Preserved). N Engl J Med. 2021;385(16):1451–1461. PubMed