Effect of Low-Dose Colchicine on Inflammatory Markers Post-Myocardial Infarction: A Randomized Controlled Trial

Abstract

Background: Myocardial infarction (MI) triggers a profound systemic and localised inflammatory response that contributes to adverse left ventricular remodelling and increased risk of recurrent cardiovascular events. Colchicine, a well-established anti-inflammatory agent with a pleiotropic mechanistic profile, has emerged as a promising adjunctive therapy in the post-MI setting. This randomized controlled trial evaluated the effect of low-dose colchicine on serial inflammatory biomarkers and cardiac functional parameters in patients with acute MI in an Egyptian tertiary care population. Methods: A prospective, double-blind, placebo-controlled, randomized trial was conducted at Badr University Faculty, Egypt. One hundred and twenty patients with acute MI (STEMI or NSTEMI) were randomized 1:1 to receive colchicine 0.5 mg twice daily for 30 days (n=60) or matching placebo (n=60), commencing within 24 hours of hospital admission, in addition to standard guidelinedirected medical therapy. The primary outcome was the change in high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), interleukin-1 beta (IL-1β), and tumour necrosis factor-alpha (TNF-α) at 72 hours and 30 days from baseline. Secondary outcomes included left ventricular ejection fraction, pericardial effusion, post-MI pericarditis, and major adverse cardiovascular events (MACE) at 30 days. Safety and tolerability were systematically assessed. Results: Both groups were well matched at baseline. At 72 hours, hs-CRP was significantly lower in the colchicine group compared with placebo (9.1 ± 3.8 vs 15.6 ± 5.4 mg/L; p<0.001). Reductions in IL-6 (21.4 ± 8.3 vs 36.9 ± 12.6 pg/mL; p<0.001), IL-1β (4.2 ± 1.8 vs 7.6 ± 2.9 pg/mL; p<0.001), and TNF-α (14.3 ± 5.4 vs 21.8 ± 7.7 pg/mL; p<0.001) were similarly significant. At 30 days, colchicine maintained markedly lower levels of all inflammatory markers compared with placebo (all p<0.001). LVEF at 30 days was significantly higher in the colchicine group (52.7 ± 6.4% vs 49.4 ± 7.1%; p=0.038). Post-MI pericarditis was significantly less frequent with colchicine (3.3% vs 13.3%; p=0.041). Gastrointestinal adverse events were numerically more frequent in the colchicine group (23.3% vs 10.0%; p=0.058), though not statistically significant. Conclusion: Low-dose colchicine administered within 24 hours of acute MI significantly attenuated the postinfarction inflammatory cascade across multiple biomarker axes at both 72 hours and 30 days, with a concomitant improvement in left ventricular systolic function and a significant reduction in post-MI pericarditis. These findings support the adjunctive use of colchicine in the early post-MI period and contribute further evidence to the growing body of research establishing the central role of inflammation in post-MI pathophysiology.