Reduction of clonal hematopoiesis mutation burden in coronary patients treated with low-dose colchicine
Tardif, J.-C.; Busque, L.; Geoffroy, S.; Sandoval, J.; Lemieux Perreault, L.-P.; Mongrain, I.; Valois, D.; Gaulin-Marion, M.-J.; Buscarlet, M.; Provost, S.; Maggioni, A. P.; Kouz, S.; Pinto, F. J.; Lopez-Sendon, J.; Waters, D. D.; Diaz, R.; Gamra, H.; Kiwan, G. S.; Berry, C.; Koenig, W.; Gregoire, J. C.; L'Allier, P. L.; Provencher, M.; Guertin, M.-C.; Roubille, F.; Oussaid, E.; Barhdadi, A.; Dube, M.-P.
Show abstract
Clonal hematopoiesis involves mutations in hematopoietic stem/progenitor cells, which increase the risk of cardiovascular disease, particularly under pro-inflammatory conditions. This study assessed the impact of the anti-inflammatory medication colchicine on clonal hematopoiesis in patients with recent myocardial infarction from the COLCOT trial. Participants were randomly assigned to low-dose colchicine (0.5 mg daily) or placebo, with 848 providing two DNA samples for longitudinal analysis. Targeted error-corrected sequencing was used, and 15,919 mutations were followed over a median period of 19.5 months. The results showed significantly lower variant allele fractions in the colchicine group compared to placebo (p interaction=0.03), with notable reductions in TET2 (10.3%, p=0.007; p interaction=0.001), TP53 (11.8%, p=0.001; p interaction=0.03), and SF3B1 mutations (19.9%, p=0.006; p interaction=0.005). Thus, colchicine reduced the proportion of clonal hematopoiesis mutations in patients with coronary disease, and longer-term studies with diverse populations are needed to confirm its potential benefits in mitigating related health risks.
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