Colchicine prevents accelerated atherosclerosis in TET2 -mutant clonal haematopoiesis
Authors' conclusion
These results highlight the potential value of colchicine to mitigate the higher cardiovascular risk of carriers of somatic TET2 mutations in blood cells.
Study context
- Population
- Ldlr-/- mice with ≈10% Tet2-/- haematopoietic cells on high-cholesterol diet; humans with whole-exome sequencing in 2 biobanks37,181 MGB + 437,236 UK Biobank
- Comparison
- Colchicine vs Placebo
- Outcome
- Accelerated atherosclerosis associated with TET2-mutant CH; modification by colchicine of the CH–MI association in humans
Methodological detailsmouse model (bone marrow transplantation in Ldlr-/- mice), human biobank analysis (Mass General Brigham Biobank, UK Biobank)
- Mouse model (bone marrow transplantation in Ldlr-/- mice)
- Human biobank analysis (Mass General Brigham Biobank, UK Biobank)
Main finding
As reported in the abstract
- Colchicine prevented accelerated atherosclerosis in the mouse model of TET2-mutant clonal haematopoiesis (CH), with suppression of interleukin-1β overproduction
- Humans prescribed colchicine had attenuated associations between TET2 mutations and MI
- Interaction not observed for other mutated genes
Original publication
Colchicine prevents accelerated atherosclerosis in TET2 -mutant clonal haematopoiesis. Eur Heart J. Published 30 August 2024. doi:10.
Summarised from the published abstract; every number is checked against it