Key result
Colchicine fails to reduce platelet reactivity compared with placebo in stable CAD.
Why the study?
Although colchicine reduces cardiovascular events in patients with CAD, the mechanisms underlying these benefits are not fully understood, and a potential antiplatelet effect remains an unproven hypothesis.
Does low-dose colchicine (0.5 mg once daily) influence platelet reactivity in stable post-myocardial infarction patients with chronic coronary artery disease on aspirin therapy?
RCT (n=80)
Double-blind
Block randomization (two blocks of 40 patients at a 1:1 ratio)
Does low-dose colchicine (0.5 mg once daily) influence platelet reactivity in stable post-myocardial infarction patients with chronic coronary artery disease on aspirin therapy?
Low-dose colchicine does not affect platelet reactivity in stable patients with chronic coronary artery disease on aspirin, suggesting its cardiovascular benefits are not mediated by antiplatelet effects.
Background Inflammation plays an important role in the development of atherosclerosis and the occurrence of ischemic events. In addition to inflammation, thrombosis is also directly involved in the pathogenesis of acute coronary syndromes. Colchicine has effects on cell adhesion molecules and inflammatory chemokines, in addition to suppressing interleukin 1. In patients with coronary artery disease (CAD), there is convincing evidence showing a decrease in cardiovascular events with the use of colchicine. However, the mechanisms behind these benefits are not fully understood, with the antiplatelet effect of the drug remaining a hypothesis. Objective The main objective of the study was to analyze the role of low dose colchicine on platelet reactivity (PR), utilizing Multiplate aggregometry with thrombin receptor-activating peptide (Multiplate TRAP). The main secondary endpoints were the analysis of PR using Multiplate adenosine diphosphate (Multiplate ADP) and Multiplate aspirin (Multiplate ASP). Methods This is a prospective, randomized, double-blind, placebo-controlled study. Eighty patients with proven chronic CAD (72.5% males, mean age 62.75 years) were randomized to receive colchicine 0.5mg once daily (intervention group, N=40) or placebo (placebo group, N=40). All patients were taking aspirin 100 mg daily. Randomization was carried out in two blocks of 40 patients at a rate of 1:1. Blood samples were collected at baseline visit and the end of follow-up (30 ± 3 days). Results The figure shows the median difference (25th,75th percentiles) in PR between baseline and follow-up for the colchicine and placebo groups, considering the three methods utilized. The median differences between the groups were, respectively, 7.0 AU (-8.75 to 22.0) vs -3.5 AU (-14.75,12.5) considering Multiplate TRAP, -1.0 AU (-17.5,22.5) vs 2.5 AU (-10.0,22.5) by Multiplate ADP analysis, and 1.5 AU (-6.5,9.75) vs. -1.0 AU (-10.5,8.00) by Multiplate ASP. Conclusion In this population of stable patients with CAD, colchicine did not influence platelet reactivity, indicating that modulation of platelet reactivity is unlikely to be a major contributor to the clinical benefit previously demonstrated with the drug.
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Andrade et al. (2026) conducted an RCT in Stable post-myocardial infarction / chronic coronary artery disease (n=80). Colchicine vs. Placebo was evaluated on Change in platelet reactivity from baseline to follow-up utilizing Multiplate aggregometry with thrombin receptor-activating peptide (Multiplate TRAP). Colchicine 0.5 mg daily did not influence Multiplate TRAP platelet reactivity compared with placebo in stable CAD patients (median change 7.0 vs -3.5 AU).
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