Colchicine did not reduce pericoronary inflammation by FAI after 12 months but was associated with increased coronary artery calcium score (92.4 to 158.4, p=0.025).
Does colchicine 0.5 mg/day reduce pericoronary inflammation measured by FAI in patients with elevated baseline FAI?
Colchicine 0.5 mg/day for 12 months did not significantly reduce pericoronary inflammation measured by FAI, but was associated with increased coronary artery calcium score and total plaque volume, suggesting a potential role in plaque stabilization.
Absolute Event Rate: 0% vs 0%
Abstract Inflammation plays a key role in atherogenesis in coronary disease. Studies confirm the prognostic value of measuring pericoronary adipose tissue (PCAT) attenuation, highlighting its correlation as an early inflammatory biomarker in atherogenesis. Colchicine, a well-documented anti-inflammatory drug with proven cardiovascular benefits, may contribute to reducing the Fat Attenuation Index (FAI) assessed via coronary computed tomography angiography (CTA). This study investigates colchicine impact on coronary inflammation reduction after 12 months of treatment. Methods: A pilot single-center, randomized, prospective, observer-blinded trial conducted in a large tertiary hospital. Forty patients with FAI ≥ -70.1 HU in the right coronary artery (RCA) and/or left anterior descending artery (LAD) were randomized to receive colchicine 0.5 mg/day for 12 months or standard care alone. The primary outcome was FAI quantification in both groups (colchicine and control) after 12 months. Secondary outcomes included assessment of changes in total atheroma volume, calcium score, progression or regression of high-risk plaques, low attenuation plaque volume variation and clinical outcomes. Results: A total of 40 patients were enrolled between May 2021 and April 2023 and 34 patients completed 1-year follow-up. Mean age was 62,5 ± 8,6 years in Colchicine group and 66,2 ± 9,7 years in Control group and both groups had similar demographic, laboratory and drug therapy characteristics. No significant FAI reduction in RCA and LAD was observed after 12 months. In the Colchicine group, the mean initial LAD FAI of -70.37 ± 7.1 HU changed to -71.48 ± 7.3 HU (p = 0.74), while the Control group showed a shift from -69.13 ± 7.7 HU to -73.45 ± 6.9 HU (p = 0.057). RCA FAI moved from -67.69 ± 5.4 HU to -70.0 ± 7.0 HU (p = 0.17) in the Colchicine group and from -65.48 ± 5.5 HU to -71.2 ± 8.8 HU (p = 0.059) in the Control group. No difference was found in the evaluation of the FAI Delta between the Colchicine and Control groups in the analyzed arteries (Δ LAD -0.74 ± 9.5 vs - 5.2 ± 9.7, p = 0.18; Δ RCA -2.4 ± 7.7 vs - 4.7 ± 8.9, p = 0.42 and Δ CX 0.45 ± 10 vs -5.2 ± 10.5, p = 0.13). Colchicine use was associated with a higher coronary artery calcium score (92.4 ± 160 to 158.4 ± 265, p=0.025) and a higher total volume plaque (73.3 ± 126 to 124.4 ± 214, p = 0.037). Conclusion: Pericoronary inflammation measured by FAI did not differ among participants who received colchicine compared to control after 12 months of treatment. Colchicine treatment was associated with a higher coronary artery calcium score, considered a feature of plaque stability. As a groundbreaking study, it establishes a foundation for future, more comprehensive research investigating alternative anti-inflammatory therapies.
Barbosa et al. (Sat,) reported a other. Colchicine did not reduce pericoronary inflammation by FAI after 12 months but was associated with increased coronary artery calcium score (92.4 to 158.4, p=0.025).