Cardiovascular Research · Nov 7, 2026
Colchicine in chronic coronary artery disease: effects on vascular glucose uptake, inflammation, remodeling and blood pressure
By Baldwin SN, Bastrup JA, Muroke V et al.
Aims: The mechanisms underlying colchicine’s cardiovascular benefits in patients with coronary artery disease remain unclear and warrant further translational investigation. Methods and results: In a randomized, double-blind, placebo-controlled trial, 111 patients with chronic coronary artery disease and aortic or carotid target-to-background ratio ≥1.6 were assigned to colchicine 0.6 mg daily (n=55) or placebo (n=56) for 24 weeks. Arterial inflammation was assessed using 18F-fluorodeoxyglucose positron emission tomography (FDG-PET) of the ascending aorta. The primary endpoint was the change in mean maximum target-to-background ratio over 24 weeks. Secondary and exploratory objectives included evaluation of systemic inflammatory markers and blood pressure. To support interpretation of the clinical findings, a complementary hypertensive rodent model, the spontaneously hypertensive rat (SHR), was treated with colchicine for 4 weeks to explore vascular and inflammatory pathways potentially influenced by colchicine using immunohistochemistry, myography and proteomics. Colchicine did not reduce aortic FDG uptake compared with placebo (adjusted mean change 0.05 [95% CI −0.02 to 0.12] vs 0.01 [95% CI −0.06 to 0.08]; p=0.38). In secondary and exploratory analyses, colchicine was associated with a reduction in neutrophil-to-lymphocyte ratio (adjusted mean change −0.36 vs −0.08; p=0.033), a trend toward lower high-sensitivity C-reactive protein (adjusted geometric mean percentage change −28.2% vs −5.8%; p=0.060) and attenuation of increases in systolic (adjusted mean change 0.88 mmHg vs. 4.94 mmHg; p=0.046) and diastolic (1.41 mmHg vs. 4.35 mmHg; p=0.048) blood pressure. In SHRs, colchicine had no effect on the aorta but attenuated the progression of hypertension and reduced inflammation and extracellular matrix remodelling in mesenteric resistance arteries, while enhancing vasodilator responses. Reductions in CXCL10, CXCL2, NLRP3 and IL-18 expression were observed in mesenteric arteries from the SHR following colchicine treatment. Conclusions: These findings support the hypothesis that vascular effects of colchicine likely extend beyond large conduit arteries, while the specific pathways and relevance to coronary atherosclerosis require further investigation.