Background/Purpose: Patients with gout experience
both inflammation and increased risk of cardiovascular disease (CVD). Studies
suggest that colchicine reduces myocardial infarction (MI) risk, but whether
colchicine reduces incident coronary artery disease (iCAD),
vs. acute plaque disruption/inflammation, is unknown. We assessed colchicine’s
impact on iCAD in gout patients.

Methods: Patients with gout or hyperuricemia
(2000-2009) were identified by ICD-9 code.  We then included only subjects
with 1) microscopic diagnosis of urate crystals; 2)
6/12 ACR gout classification criteria, 3) rheumatologist gout diagnosis; or 4)
4-5 ACR criteria plus a PCP gout diagnosis. Patients with a diagnosis of CAD at
index date were excluded. Pharmacy records distinguished colchicine users (1
period of prescription for >30 days) vs non-users.
Chart review identified iCAD, defined as first
positive cardiac stress test or cardiac catheterization, PCI (stent or
angioplasty) or CABG. Incident MI was also recorded.

Results: Of 7,819 patients with an ICD-9 diagnosis of
gout/hyperuricemia, 446 colchicine users and 278
non-users met inclusion criteria (2,118 vs. 1,367 years of follow-up for
colchicine vs control group). Baseline
characteristics were generally similar across groups (Table 1). We found no
increased iCAD prevalence among colchicine users vs non-users (Table 2). Inclusion of incident MI as a
criterion for iCAD did not result in any significant
difference between the groups. When expressed as incidence rate (events per
patient-years), iCAD again did not vary between
groups. The individual components of the outcome were also similar between the
two groups (not shown). In multivariate models, after controlling for potential
variables, colchicine use still did not impact the risk of iCAD.

Conclusion: Our data suggest that chronic colchicine
use does not impact the rate of iCAD in gout
patients. In conjunction with prior studies suggesting a reduction in acute
cardiovascular events among colchicine users, our data suggest that colchicine
is likely to act by preventing acute events (e.g., plaque rupture, or vascular
occlusion post-plaque rupture), rather than by reducing iCAD.

Supported by an investigator-initiated grant from Takeda,
Inc.