Arrhythmias & electrophysiologyCohort study
A proteomic analysis of atrial fibrillation in a prospective longitudinal cohort (AGES-Reykjavik study)
- Prospective cohort study
- population-based
- bidirectional two-sample Mendelian randomization
Authors' conclusion
The AF proteomic signature includes biologically relevant proteins, some of which may be causal. It mainly reflects an NT-proBNP-dependent consequence of the genetic liability to AF. N-terminal prohormone of brain natriuretic peptide is a promising marker for incident AF in the short term, but risk assessment incorporating a PRS may improve long-term risk assessment.
Study context
- Population
- Older adults in the population-based AGES-Reykjavik study; 4137 serum proteins vs incident atrial fibrillation (AF)1,172 developed AF
- Participants
- 4,765 adults
- Outcome
- Incident AF (associations with 4137 baseline serum proteins)
Main finding
As reported in the abstract
Proteins in the AF signature
76
Novel proteins
63 (83%)
Replicated in Cardiovascular Health Study (CHS)
29 (38%)
Causal candidates (TAGLN, WARS, CHST15, CHMP3, COL15A1, DUSP13, MANBA, QSOX2, SRL)
Nine
Observational data: associations, not effects.
Further findings
Reverse causal analysis
- Most AF-associated proteins affected by genetic liability to AF
Prediction of incident AF (time-dependent AUC)
- N-terminal prohormone of brain natriuretic peptide (NT-proBNP) improved prediction of incident AF close to baseline; AF-PRS gave further improvements at all time points
Original publication
Summarised from the published abstract; every number is checked against it