Can colchicine tame atrial fibrillation? A scoping review

Background Emerging evidence identifies inflammation as a key contributor to the initiation and maintenance of atrial fibrillation (AF). Activation of the nucleotide-binding oligomerisation domain-like receptor pyrin domain containing protein 3 (NLRP3) triggers the downstream release of pro-inflammatory cytokines that may promote atrial structural and electrical remodelling, contributing to the pathogenesis of AF. Colchicine inhibits NLRP3 activation and may hold a therapeutic role in reducing AF incidence and recurrence (Figure 1). Aim To map existing literature on the role of inflammation in the pathogenesis of AF and evaluate colchicine as a therapeutic option for reducing AF events. Method A scoping review was conducted as per the PRISMA-ScR framework. Predefined inclusion and exclusion criteria guided comprehensive MEDLINE and Embase searches. Literature published between 2015–2025 on adults (≥18) with new-onset AF investigating inflammation or colchicine was reviewed, and data were charted thematically to identify knowledge gaps. Critical appraisal employed the JBI Critical Appraisal checklists for clinical studies and the AMSTAR 2 for systematic reviews. Results The research addressed 35 studies comprising meta-analyses, systematic reviews and randomised controlled trials. The study population consisted mainly of post-cardiac surgery (40%) and post-catheter ablation for AF (48.6%) (Table 1). Primary outcomes measured were AF occurrence, gastrointestinal (GI) side effects and treatment discontinuation. Colchicine doses varied between 0.3–2 mg, once or twice daily, for 7 days to 7 months. The follow-up ranged from 7 days to 34 months. Across the included studies, colchicine consistently demonstrated reduced incidence of AF, with effect estimates ranging from OR 0.2–0.85, HR 0.78–0.98, and RR 0.54–0.75. Mechanistic studies supported these findings, indicating that colchicine mitigates NLRP3-driven inflammation, reducing pro-arrhythmic atrial remodelling including fibrosis and ionic channel modulation. GI adverse effects, primarily diarrhoea, occurred in 5.1%–26.8% of colchicine-treated patients compared to 1%–11.8% in the placebo groups (p=0.00001–0.05). Two studies reported higher discontinuation rates with colchicine (12.5%–14.9%) in comparison to the placebo groups (4.9%–10.8%), although, one study observed improved tolerability with lower-dose (0.5 mg) and longer-duration regimens (10 days). Conclusion Colchicine reduces the incidence of AF in post-cardiac surgery and post-AF ablation cohorts but increases GI adverse effects. Given the shared NLRP3-activated inflammatory mechanisms implicated in non-surgical AF, further investigation of colchicine as a therapeutic option in this population is warranted, as current data remain limited. Moreover, due to the heterogeneity among existing trials, future studies should aim to define the optimum dose and treatment duration at which colchicine confers maximal benefit in reducing AF risk.Table 1Figure 1