Background & Objective: Colchicine improves cardiovascular outcomes in patients with coronary heart disease, but the underlying mechanisms remain incompletely elucidated. The aim of this study was to evaluate the effects of colchicine on systemic inflammation, peripheral blood CD4⁺ T cell subsets, and oxidative stress after percutaneous coronary intervention in patients with coronary heart disease combined with gout from the perspective of population study. Methods: From January 2019 to June 2022, a total of 128 patients with coronary heart disease combined with gout who underwent percutaneous coronary intervention (PCI) at our hospital were retrospectively collected and divided into colchicine group (n = 64) and control group (n = 64) according to whether colchicine was routinely used or not. Systemic inflammation (tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and hypersensitivity C-reactive protein (hs-CRP)), peripheral blood CD4⁺ T cell subsets (Th1 cells, Th17 cells, and regulatory T cells), and oxidative stress indicators (serum superoxide dismutase (SOD) and malondialdehyde (MDA)) were compared between the two groups after PCI. hs-CRP ≥2 mg/L was defined as a patient at risk of residual inflammatory. Logistic regression was used to analyze the association between colchicine treatment and the risk of residual inflammation. Results: There was no significant difference between the two groups in terms of age, gender, smoking history, disease history, body mass index (BMI), time from symptom onset to PCI, blood pressure, hypersensitivity troponin I (hs-TnI), neutrophils, triglyceride (TG), total cholesterol (TC), low density lipoprotein cholesterol (LDL-C), serum creatinine, and the equilibrium was comparable (p > 0.05). After PCI treatment, TNF-α and IL-6 levels were significantly decreased in both groups, and the levels of TNF-α and IL-6 in the colchicine group were significantly lower than control group (TNF-α: 22.5 ± 4.9 vs 41.6 ± 4.1 μg/L; IL-6: 21.3 ± 12.8 vs 40.9 ± 17.5 ng/L; both p < 0.001). Patients in the colchicine group had a significantly proportion of risk of residual inflammation compared with controls (37.5% vs 62.5%, p = 0.005). Logistic regression showed that, using the control group as a reference, we still found that colchicine use was independently associated with a reduced risk of residual inflammation when corrected for other confounders (odds ratio [OR], 0.372; 95% confidence interval [CI], 0.156–0.889; p = 0.026). Regarding peripheral blood CD4⁺ T cell subsets, Th1 cell, Th17 cell, and regulatory T cell counts were significantly higher in the colchicine group than control group after PCI treatment (p < 0.01). As for oxidative stress indicators, SOD levels were significantly higher and MDA levels were significantly lower in the colchicine group after PCI treatment compared with the control group (p < 0.001). Conclusions: Colchicine administration was associated with reduced systemic inflammatory indexed, promoted proliferation of peripheral blood CD4⁺ T cells, and improved oxidative stress levels in patients with coronary heart disease combined with gout after PCI.