Background/Purpose: Atherosclerosis is an inflammatory process, but to date no anti-inflammatory agent has definitively been shown to alter cardiovascular (CV) risk. Colchicine is an anti-inflammatory agent that inhibits macrophages, endothelial cells, and neutrophils, all implicated in atherosclerosis. In a cross-sectional study, we found that colchicine use was associated with reduced prevalence of myocardial infarction (MI) in gout patients [1]. To further evaluate the relationship between colchicine and CV risk, we initiated a retrospective cohort study. Here we present an interim analysis.

Methods: We identified all active New York Harbor VA patients with an assigned ICD-9 code for gout or hyperuricemia between 2000-09. Charts were manually screened to confirm a diagnosis of gout utilizing ACR criteria, and pharmacy records were used to identify subjects on daily colchicine for ≥ 30 days (colchicine group). Subjects receiving no colchicine prescriptions formed the control group. Baseline characteristics including CV risk factors and medication use were ascertained. We excluded patients who did not meet our diagnostic criteria for gout, who received as-needed colchicine only, or with ≤ 3 months of follow-up time available for evaluation. We defined colchicine lapse as any period of non-colchicine use beginning 2 weeks after medication cessation (to account for the elimination time of the drug). The primary outcome was MI during the study period.  

Results: 7819 subjects had requisite ICD-9 codes. Among 1031 charts reviewed to date, 214 patients met gout criteria and 183 were enrolled. Of these, 121 subjects (66%) used colchicine (totaling 363.8 patient-years of exposure) and 62 subjects (34%) used no colchicine (totaling 249.8 patient-years of follow-up). Colchicine and control groups had similar rates of hypertension (0.85 vs 0.92, p=0.2), diabetes (0.37 vs 0.3, p=0.4), hyperlipidemia (0.66 vs 0.56, p=0.3), coronary artery disease (0.29 vs 0.37, p= 0.3), and allopurinol use (0.22 vs 0.21, p= 1.0), as well as similar BMI (30.6 vs 29.8, p=0.3), serum urate (8.4 vs 8.2 mg/dL, p=0.6), and creatinine (1.3 vs 1.4 mg/dL, p=0.7). Colchicine users experienced no MIs while on their medication. In contrast, control patients had 4 MIs (0 vs 6.4%; p=0.01), and 3 MIs occurred during colchicine lapses (3%; lapse vs colchicine p=0.09; lapse vs control p=0.43; mean time from last colchicine use to MI 5.9 months). We also compared rates of MI per patient-year between colchicine exposure (0.0), control follow-up (0.016), and colchicine lapse follow-up (0.018) periods, and observed significant differences between colchicine vs control (p=0.036) and colchicine vs lapse (p=0.035), but not between control vs lapse group MI rates (p=0.26). 

Conclusion: In this interim analysis, gout patients taking colchicine had a significantly reduced rate of MI vs non-users, and vs themselves during periods when not taking colchicine. These data suggest that colchicine is protective against MI, though probably only during active use. Evaluation of the remaining 6,788 patients is ongoing.

[1] Crittenden DB et al. J Rheum 2012 E Pub.

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ACR Meeting Abstracts - https://acrabstracts.org/abstract/colchicine-is-associated-with-a-decreased-rate-of-myocardial-infarction-in-gout-patients-interim-results-from-a-retrospective-cohort-study/