Heart failure & cardiomyopathiesCase-control study
Proteomics Profiling Reveals Circulating Biomarkers and Dysregulated Pathways in Transthyretin Amyloid Cardiomyopathy
- case-control study
- age- and sex-matched
- training set 70% / internal test set 30%
- external validation
Authors' conclusion
This study reveals a distinct proteomic profile of ATTR-CM compared with controls with HF, and elucidates both novel and known signaling pathways that are differentially regulated in ATTR-CM.
Study context
- Population
- Cases with ATTR-CM, internal controls with hypertensive left ventricular hypertrophy, and external controls with heart failure (HF)controls: 170 internal controls with hypertensive left ventricular hypertrophy and 50 external controls with HF · ATTR-CM cases 169 · internal controls with hypertensive left ventricular hypertrophy 170 · external controls with HF 50
- Participants
- 169 cases and 220 controls cases
- Comparison
- Proteomics-based discrimination model distinguishing ATTR-CM cases from controls
- ATTR-CMn = 169
- internal controlsn = 170
- external controlsn = 50
Main finding
As reported in the abstract
Discriminant proteins identified in the training set
discriminant proteins
211
Observational data: associations, not effects.
Further findings
Discrimination of ATTR-CM in the test set from external controls with HF
- area under the receiver-operating characteristic curve
- 0.89 (95% CI, 0.82-0.96)
- sensitivity
- 0.90 (95% CI, 0.75-0.97)
- specificity
- 0.86 (95% CI, 0.72-0.96)
Pathway analysis
- PI3K-Akt pathway and related pathways (eg, JAK-STAT) dysregulated
- Dysregulation of complement and coagulation cascade pathways
- false discovery rate <0.05 declared positive
Original publication
Proteomics Profiling Reveals Circulating Biomarkers and Dysregulated Pathways in Transthyretin Amyloid Cardiomyopathy. Circ Heart Fail. Published 22 January 2026. doi:10.1161/circheartfailure.125.013220
Summarised from the published abstract; every number is checked against it