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Final Program


Program-At-A-Glance

Rapid Fire Session

Session: Rapid Fire Session 5: CMR - Analysis (including machine learning) (Monitor 6)

Leptin and Heart Failure Phenotypes: Associations With Cardiac Magnetic Resonance Markers, Exercise Performance, and microRNAs

Saturday, February 7, 2026
10:22 AM - 10:29 AM  
Location: Galapagos / Aruba / Ilhabela (2nd Lower Level)
Background: Background: Increased body mass index (BMI) is a well-established risk factor for heart failure (HF). Interestingly, obese patients with HF may paradoxically present better outcomes than leaner individuals, a phenomenon known as the “obesity paradox.” Leptin, an adipokine central to energy balance, may participate in cardioprotective pathways, potentially through the regulation of microRNAs (miRNAs). To explore the relationship between plasma leptin levels, myocardial remodeling assessed by cardiac magnetic resonance (CMR) including T1 mapping, and functional capacity evaluated by cardiopulmonary exercise testing (CPET) in distinct HF phenotypes

Methods: Patients with symptomatic HF (NYHA class ≥ II) were prospectively enrolled and categorized into HF with reduced ejection fraction (HFrEF, LVEF < 45%) or preserved ejection fraction (HFpEF, LVEF ≥45%). All participants underwent blood sampling, 3T CMR (Achieva, Philips Medical Systems) with cine steady-state free precession imaging and T1 mapping for extracellular volume (ECV), and CPET to determine peak VO₂ and ventilatory efficiency. Plasma leptin was measured using ELISA.

Results: The study included 65 patients: 29 non-obese (BMI < 30 kg/m²) and 36 obese (BMI ≥30 kg/m²). Obese patients exhibited higher plasma leptin (p=0.002) and NT-proBNP (p=0.036), whereas indexed left ventricular mass (LVMi) was greater in non-obese patients (p=0.023). Obese individuals also showed higher peak VO₂ (p=0.012) but reduced ventilatory efficiency (p=0.034).

Correlation analyses revealed inverse associations of leptin with LVMi (r=-0.321, p=0.023) and adjusted peak VO₂ (r=-0.365, p=0.012), and a positive association with myocardial ECV (r=0.301, p=0.042). Subgroup analysis showed phenotype-specific patterns. In HFrEF, leptin correlated inversely with LVMi (r=-0.463, p=0.023), adjusted peak VO₂ (r=-0.416, p=0.043), and troponin (r=-0.454, p=0.022). In HFpEF, leptin correlated positively with ECV (r=0.407, p=0.049) and LVEF (r=0.407, p=0.039).

Conclusion: Plasma leptin demonstrated distinct and clinically meaningful associations with myocardial structure, tissue remodeling, and exercise performance across HF phenotypes. In HFrEF, inverse correlations with LV mass and troponin suggest a potential protective role, whereas in HFpEF, positive correlations with ECV and LVEF point toward alternative remodeling pathways. These results emphasize leptin, potentially regulated by miRNAs, as a mediator of myocardial remodeling and functional adaptation in HF. Understanding these mechanisms may help clarify the paradoxical impact of obesity in HF and guide novel strategies for risk stratification and therapy.