Heart failure & cardiomyopathies
Myeloid Cell Expansion Propels Right Ventricular Dysfunction in Heart Failure with Preserved Ejection Fraction (HFpEF) Through Sterile Inflammation
Authors' conclusion
We demonstrate that dysregulated myeloid cell dynamics are associated with, and directly contribute to, the pathogenesis of RVD associated with HFpEF in humans and mice.
Study context
- Population
- Young (<20-week-old) and aged (>80-week-old) male and female C57BL/6J mice; patients with HFpEF (right ventricular (RV) biopsies)
- Comparison
- Chow vs HFpEF vs Chronic hypoxia vs RV-HFpEF
Methodological detailsmurine HFpEF model, human RV biopsies
- Murine HFpEF model
- Human RV biopsies
Main finding
As reported in the abstract
- RV-HFpEF: LV diastolic dysfunction (increased E/E' ratio, reduced global longitudinal peak strain, smaller end-diastolic diameters, increased isovolumetric relaxation time) vs chow
- RV-HFpEF: RV hypertrophy and RVD (increased Fulton index, elevated RV systolic pressure, reduced TAPSE)
- Total leukocyte, monocyte and macrophage counts elevated in RV tissue of RV-HFpEF mice vs chow RV tissue and LV tissue of young and aged RV-HFpEF animals
- Proteomics: increased abundance of proteins of innate immune activation, macrophage chemotaxis and leukocyte migration in RV tissue of RV-HFpEF mice
- Fate mapping: recruited monocyte-derived macrophages main source of cardiac macrophages in RV tissue of RV-HFpEF mice
- Myeloid cell depletion (CSF1R inhibitor) associated with lower RVSP in RV-HFpEF mice vs controls
- Human HFpEF RV biopsies: increased adhesion molecules, fibrotic markers and inflammatory transcripts; association between RVD and CD68+ cells
Original publication
Myeloid Cell Expansion Propels Right Ventricular Dysfunction in HFpEF Through Sterile Inflammation. Circulation. Published 18 August 2026. doi:10.
Summarised from the published abstract; every number is checked against it