Heart failure & cardiomyopathiesSecondary analysis
Coordinated Expression of BMP10/ALK1/endoglin—Proteins that Drive Embryonic Cardiac and Vascular Morphogenesis—in Patients with Heart Failure: The EMPEROR Program
- Secondary analysis of the EMPEROR Program trials
- two distinct cohorts
Authors' conclusion
The coordinated circulating expression of proteins critical to foetal cardiac and vascular development tracks closely with the severity of heart failure, as reflected by symptoms, cardiac injury and stress, prevalence of atrial fibrillation and other comorbidities, and prognosis, suggesting a role of BMP10/ALK1/endoglin signalling in the progression of heart failure.
Study context
- Population
- Patients with HF in the EMPEROR Program
- Participants
- 1,127 vs 1,120
- Comparison
- Tertiles of circulating BMP10, ALK1 and endoglin
- Cohort 1n = 1,127
- Cohort 2n = 1,120
- Primary endpoint
- Major adverse HF events
Primary result
As reported in the abstract
Increasing BMP10, ALK1 and endoglin levels associated with progressively higher risks of major adverse outcomes (all three proteins, all HF endpoints)
p for trend <0.001
Further findings
Baseline characteristics
- Higher BMP10, ALK1 and endoglin associated with worse functional class, higher likelihood of AF and higher natriuretic peptides and troponin T
- P for trend < 0.001
- Levels at baseline and changes during follow-up closely correlated with each other
Effect of empagliflozin on BMP10
- Modest reduction of BMP10 with empagliflozin in both cohorts
Original publication
Summarised from the published abstract; every number is checked against it