Restenosis following coronary artery stenting remains a significant clinical problem, particularly in patients with ischemic heart disease. Although the introduction of drug-eluting stents (DES) has reduced the incidence of restenosis, certain subgroups—including patients with diabetes mellitus and vascular calcification—continue to experience high rates of in-stent restenosis, leading to recurrent ischemia and adverse cardiovascular events.Inflammation plays a central role in the development of restenosis. The vascular injury caused by stent implantation triggers an inflammatory cascade that promotes neointimal proliferation and vessel re-narrowing. Colchicine, a well-known anti-inflammatory agent, has demonstrated efficacy in modulating the NLRP3 inflammasome and reducing systemic inflammation markers such as C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α). However, its role in preventing restenosis after PCI remains incompletely defined.The aim of our study was to assess the efficacy of colchicine in reducing the incidence of restenosis at one year following coronary stenting in patients with ischemic heart disease. Specific objectives included:
(1) comparing restenosis rates at 12 months between patients receiving colchicine and those receiving placebo;
(2) evaluating the effect of colchicine on inflammatory markers (CRP, IL-6, TNF-α) before and after treatment;
(3) conducting subgroup analyses in patients with diabetes mellitus and vascular calcification to determine colchicine’s efficacy in these high-risk groups;
(4) assessing the impact of colchicine therapy on major adverse cardiovascular events (MACE) during one-year follow-up; and
(5) analyzing restenosis distribution across different coronary arteries (LAD, RCA, LCX) and identifying anatomical factors associated with disease progression.

his was a prospective, randomized, controlled trial conducted at Ezgu Niyat Cardiology Center and Carmen+ Clinic (Uzbekistan) from January 2021 to December 2024. A total of 120 patients with stable coronary artery disease (CAD) who underwent successful elective percutaneous coronary intervention (PCI) with drug-eluting stent (DES) implantation were enrolled in the study.Participants were randomly assigned in a 1:1 ratio into two groups:

• Group 1 (Colchicine Group): 60 patients received colchicine 0.5 mg once daily for 12 months.
• Group 2 (Placebo Group): 60 patients received a matching placebo following the same dosing schedule.

Inclusion criteria were age between 18 and 75 years, diagnosis of stable ischemic heart disease, and successful PCI with DES implantation.
Exclusion criteria included known allergy to colchicine, severe hepatic or renal dysfunction, recent (<1 month) myocardial infarction or stroke, and active infections.The primary endpoint was the rate of in-stent restenosis at 12 months, as confirmed by follow-up coronary angiography. Restenosis was defined as ≥50% luminal diameter narrowing within the stented segment.Secondary endpoints included the incidence of major adverse cardiovascular events (MACE) during the 12-month follow-up period, as well as changes in inflammatory biomarkers (C-reactive protein [CRP], interleukin-6 [IL-6], and tumor necrosis factor-alpha [TNF-α]) from baseline to 12 months.

At one-year follow-up, the incidence of angiographically confirmed restenosis was significantly lower in the colchicine group compared to the placebo group (6.7% vs. 18.3%, p = 0.02).In the colchicine group (n = 60), restenosis occurred in 4 patients (6.7%):

• LAD: 0/25 (0%)
• RCA: 3/20 (15%)
• LCX: 1/15 (6.7%)

Subgroup analysis revealed:

• Patients with diabetes: 3/41 (7.3%)
• Patients without diabetes: 1/19 (5.3%)
• Patients with coronary calcification: 2/26 (7.7%)

In the placebo group (n = 60), restenosis occurred in 11 patients (18.3%):

• LAD: 2/30 (6.7%)
• RCA: 5/20 (25%)
• LCX: 4/10 (40%)

Subgroup analysis showed:

• Patients with diabetes: 7/42 (16.7%)
• Patients without diabetes: 4/18 (22.2%)
• Patients with coronary calcification: 4/26 (15.4%)

Inflammatory markers:Colchicine group (n = 60):

• CRP: 4.2 ± 1.1 → 1.8 ± 0.7 mg/L
• IL-6: 6.5 ± 1.4 → 3.1 ± 1.0 pg/mL
• TNF-α: 12.7 ± 2.3 → 6.2 ± 1.5 pg/mL
  (All p < 0.01)

Placebo group (n = 60):

• CRP: 4.1 ± 1.0 → 3.9 ± 1.1 mg/L
• IL-6: 6.4 ± 1.5 → 5.8 ± 1.3 pg/mL
• TNF-α: 12.5 ± 2.0 → 10.9 ± 2.1 pg/mL
  (No significant change; p > 0.05)

Colchicine at a dose of 0.5 mg daily significantly reduced the rate of in-stent restenosis compared to placebo at one-year follow-up. These findings are consistent with previous meta-analyses highlighting the anti-inflammatory effects of colchicine and its ability to modulate vascular inflammation.Our results support current ESC and ACC guidelines that advocate the use of anti-inflammatory therapies in high-risk atherosclerotic patients, including those with diabetes mellitus and coronary calcification. In patients treated with colchicine, restenosis was nearly absent in the LAD and LCX territories, suggesting its protective role in these critical vascular segments.Patients with coronary calcification, traditionally considered at high risk for restenosis, also derived clear benefit from colchicine therapy. In contrast, the placebo group showed a significantly higher restenosis rate, particularly in individuals with calcified lesions and diabetes.These results indicate that colchicine may serve as a valuable adjunct to standard post-PCI therapy for restenosis prevention in high-risk populations. Further large-scale studies are warranted to validate these findings and refine patient selection criteria.