Heart failure & cardiomyopathies
Receptor Autoantibodies: Associations with Cardiac Markers, Histology, and Function in Human Non-Ischaemic Heart Failure
Authors' conclusion
GPCR autoantibodies are markedly altered in HF. However, they are correlated poorly or even inversely to haemodynamic, metabolic, and functional markers of disease severity, myocardial histology, and myocardial mitochondrial efficiency.
Study context
- Population
- Patients with non-ischaemic heart failure (HF) undergoing endomyocardial biopsy, and healthy controls
- Participants
- 95 vs 60
- Exposure
- Non-ischaemic HF patients vs healthy controls
- HFn = 95
- Healthy controlsn = 60reference
- Outcome
- Serum GPCR autoantibody levels in HF vs controls and their associations with serological, haemodynamic, metabolic and functional parameters in HF
Main finding
As reported in the abstract
- Autoantibodies against β1AR, M5AR and AT2R increased in HF
- all P < 0.001
- Autoantibodies against α1AR and AT1R decreased in HF
- all P < 0.001
Observational data: associations, not effects.
Further findings
Correlation of G-protein-coupled receptors (GPCR) autoantibodies with markers of cardiac or systemic inflammation, cardiac damage, haemodynamics, myocardial histology, LV inflammation (T2 mapping)
- Correlations weak, even when corrected for total IgG
β1AR autoantibodies vs LV fibrosis markers (T1 mapping) and global longitudinal strain
- Inverse relation with T1 mapping fibrosis markers
- r = −0.362, P < 0.05
- Inverse relation with global longitudinal strain
- r = −0.323, P < 0.05
AT2R autoantibodies vs myocardial mitochondrial coupling (high-resolution respirometry)
- Associated with improved mitochondrial coupling
- r = −0.352, P < 0.05
GPCR autoantibodies in insulin-resistant HF patients
- AT2R autoantibodies decreased
- r = −.240, P < 0.05
- AT1R autoantibodies increased
- r = 0.212, P < 0.05
Original publication
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