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Final Program


Program-At-A-Glance

Oral Abstracts Session

Virtual Recording

Session: Oral Abstracts Clinical Session 2

Heart Failure with Improved Ejection Fraction: CMR Comparisons with Prognostic Implications

Thursday, February 5, 2026
3:30 PM - 3:40 PM  
Location: Asia IV and Hall 8 (3rd Floor)

    Presenting Author(s)

  • Maryum Farooq, MB

    Research Fellow
    Leeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds
    Leeds, England, United Kingdom

    • Primary Author(s)

  • Maryum Farooq, MB

    Research Fellow
    Leeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds
    Leeds, England, United Kingdom

    • Co-Author(s)

  • Bradley Chambers

    Clinical Research Fellow
    University of Leeds
    Harewood, England, United Kingdom

  • TA

    Thomas Anderton, MBChB

    Clinical research fellow
    University of Leeds, Multidisciplinary Cardiovascular Research Centre and Biomedical Imaging Science Department, Leeds Institute of Cardiovascular and Metabolic Medicine, LS2 9JT, United Kingdom
    Leeds, England, United Kingdom

  • MG

    Michelle Gibbs

    Medical Student
    University of Leeds, England, United Kingdom

  • Masafumi Takafuji, MD, PhD

    Clinical Research Fellow
    Leeds Institute of Cardiovascular and Metabolic Medicine
    Leeds, England, United Kingdom

  • CS

    Ching-Hui Sia, MD

    Dr
    Leeds Institute of Cardiovascular and Metabolic Medicine, United Kingdom

  • CS

    Chin Soo, MB

    CRF
    LICAMM
    Leeds, England, United Kingdom

  • MA

    Mehak Asad, MD, MPH

    Clinical research fellow
    University of Leeds, Multidisciplinary Cardiovascular Research Centre and Biomedical Imaging Science Department, Leeds Institute of Cardiovascular and Metabolic Medicine, LS2 9JT, United Kingdom
    Leeds, England, United Kingdom

  • ML

    May Lwin, MD

    Clinical Research Fellow
    University of Leeds
    Leeds, England, United Kingdom

  • BH

    Brian P Halliday, PhD, MSc

    Clinical Associate Professor
    Cardiovascular Research Centre, Royal Brompton Hospital and National Heart Lung Institute, Imperial College, London, United Kingdom, United Kingdom

  • John Greenwood, MD, PhD, FSCMR

    Director
    Baker Heart and Diabetes Institute
    Melbourne, Victoria, Australia

  • Sven Plein, MD, PhD

    Professor of Cardiology
    Leeds Institute of Cardiovascular and Metabolic Medicine
    Leeds, England, United Kingdom

  • Peter P. Swoboda, PhD

    Consultant Cardiologist
    Leeds Institute of Cardiovascular and Metabolic Medicine
    Leeds, England, United Kingdom

Background: Heart failure with improved ejection fraction (HFimpEF) is an increasingly recognised phenotype, reflecting the success of guideline directed medical therapy (GDMT). Whilst outcomes are generally more favourable than in patients with persistently reduced ejection fraction, this heterogenous group remains vulnerable to relapse and cardiac complications. A key clinical challenge is identifying patients at low risk who may safely de-escalate GDMT versus those who require ongoing therapy and close monitoring. We aimed to compare CMR characteristics across heart failure phenotypes and identify CMR predictors of outcomes in HFimpEF to inform risk stratification.

Methods: We prospectively recruited patients with a recent diagnosis of heart failure referred for early cardiac magnetic resonance (CMR) imaging. At the time of CMR, patients were classified as having reduced ejection fraction (HFrEF, LVEF < 40%), improved ejection fraction (HFimpEF, LVEF >40% with ≥10% absolute increase from baseline), or preserved ejection fraction (HFpEF, LVEF >40% on both baseline echocardiogram and CMR). The CMR protocol included volumetric analysis, late gadolinium enhancement (LGE), motion-corrected quantitative stress/rest perfusion, and T1, T2, and extracellular volume (ECV) mapping. Patients were followed for major adverse cardiovascular events (MACE), defined as all-cause mortality or heart failure hospitalisation.

Results: A total of 686 patients were recruited. The median time from baseline echocardiogram to CMR was 98 days (IQR 54–181). Based on CMR, 240 patients (35%) were categorised as HFimpEF, 114 (17%) as HFpEF, and 332 (48%) as HFrEF. There were no significant differences in CMR parameters between the HFimpEF and HFpEF groups. The HFrEF group demonstrated a significantly higher prevalence of both ischaemic fibrosis (26% vs 13%, p < 0.001) and non-ischaemic fibrosis (36% vs 25%, p = 0.007). Median follow-up was 3.2 years (IQR 1.7–4.9). Kaplan–Meier analysis showed a significant difference in event-free survival across HF phenotypes (log-rank p = 0.004), with worse outcomes in HFrEF compared to HFimpEF (p = 0.017), but no significant difference between HFimpEF and HFpEF (p = 0.278). In multivariable Cox regression adjusted for age, sex, and diabetes, higher rest myocardial blood flow was independently associated with increased risk of MACE (HR 18.05, 95% CI 6.01–54.17, p < 0.001), while greater myocardial perfusion reserve was protective (HR 0.44, 95% CI 0.28–0.69, p < 0.001).

Conclusion: The CMR phenotype of HFimpEF was similar to HFpEF with less fibrosis than HFrEF. In patients with HFimpEF, rest myocardial blood flow and myocardial perfusion reserve were independently associated with adverse outcomes. These findings highlight the potential role of CMR in risk stratification and personalisation of therapy in patients with HFimpEF.

Table 1. CMR characteristics across heart failure phenotypes.

Variable

HFpEF

 

HFimpEF

 

HFrEF

P Value – HFimpEF vs

HFpEF

HFrEF

LVEDV indexed to BSA (ml/m2)

91 ± 19

94 ± 26

128 ± 42

0.967

< 0.001

LV EF (%)

51 ± 6

50 ± 7

29 ± 8

0.968

< 0.001

LV mass index (g/m2)

58 ± 15

62 ± 17

75 ± 21

0.143

< 0.001

RVEDV indexed to BSA (ml/m2)

78 ± 19

76 ± 19

82 ± 26

1.000

0.005

RV EF (%)

54 ± 9

54 ± 10

44 ± 13

1.000

< 0.001

Ischaemic fibrosis, n (%)

11 (10)

30 (13)

85 (26)

0.426

< 0.001

Inducible ischaemia, n (%)

6 (5)

13 (5)

29 (9)

0.945

0.137

Non-ischaemic fibrosis, n (%)

30 (26)

61 (25)

120 (36)

0.873

0.007

Global native T1 (ms)

1314 ± 46

1312 ± 47

1341 ± 53

1.000

< 0.001

Extracellular volume fraction (%)

26 ± 4

27 ± 5

28 ± 5

0.168

0.022

Global T2 (ms)

42 ± 6

42 ± 4

42 ± 3

1.000

1.000

Stress Myocardial Blood Flow (ml/g/min)

1.9 ± 0.5

1.9 ± 0.6

1.5 ± 0.6

0.367

< 0.001

Rest Myocardial Blood Flow (ml/g/min)

0.7 ± 0.2

0.7 ± 0.2

0.6 ± 0.2

0.404

0.021

Myocardial Perfusion Reserve

2.8 ± 0.9

2.7 ± 0.9

2.5 ± 1.1

1.000

0.146


Table 2. Multivariable Cox Regression for Composite Outcome of Death or HF Hospitalisation in HFimpEF (adjusted for Age, Sex, and Diabetes).

Variable

Hazard Ratio

95% CI

P value

Age

1.035

1.005-1.065

0.021

Male Sex

1.207

0.630-2.312

0.571

Diabetes

2.065

1.011-4.218

0.046

General

Heart rate

1.037

1.013-4.381

0.003

Systolic blood pressure

1.008

0.992-1.024

0.339

Baseline LVEF on echocardiography

1.010

0.962-1.061

0.679

Comorbidities

Hypertension

1.267

0.642-2.503

0.495

Hypercholesterolaemia

0.949

0.480-1.879

0.881

Cerebrovascular event

1.599

0.729-3.507

0.242

Atrial fibrillation

0.896

0.446-1.798

0.757

CMR Volumetrics

LVEDV indexed to BSA

0.991

0.976-1.005

0.199

LV EF

1.010

0.962-1.061

0.679

LV mass index

0.995

0.974-1.016

0.613

LVEDV indexed to BSA

0.996

0.978-1.015

0.690

RV EF

1.007

0.973-1.043

0.684

Tissue Characteristics

Ischaemic fibrosis

1.577

0.683-3.639

0.286

Inducible ischaemia

0.617

0.144-2.637

0.515

Non-ischaemic fibrosis

0.841

0.390-1.815

0.659

Global native T1

1.006

0.998-1.013

0.128

Extracellular volume fraction

1.046

0.988-1.107

0.124

Global T2

0.968

0.870-1.078

0.555

Myocardial Perfusion

Stress Myocardial Blood Flow

1.333

0.764-2.328

0.311

Rest Myocardial Blood Flow

18.049

6.014-54.168

< 0.001

Myocardial Perfusion Reserve

0.444

0.284-0.694

< 0.001

Corrected Rest Myocardial Blood Flow

9.611

2.410-38.324

0.001

Corrected Myocardial Perfusion Reserve

0.701

0.436-1.128

0.144


Figure 1. Kaplan-Meier survival analysis for MACE (death or heart failure hospitalisation) across heart failure phenotypes.