Aernoud Fiolet

77 Colchicine in Stable Coronary Artery Disease selected patients. 26 It seems reasonable to believe that the broad mechanism of action of colchicine might address the various inflammatory processes involved rather than one specific pathway. EVIDENCE FOR COLCHICINE IN STABLE CORONARY ARTERY DISEASE Retrospective Studies on Cardiovascular Outcomes in Gout Animal studies starting as early as the 1970s have shown that colchicine could inhibit the development of atherosclerosis independent of statin therapy and reduce the risk of stent stenosis, but clinical evidence has also re-emerged in the last decade. 27,28,29 Two retrospective observational studies examined the effect of colchicine in patients with gout (Table I). The first examined the crude association of colchicine use and incidence of myocardial infarction. 30 In a cohort of patients with gout, 576 patients had a colchicine prescription and 712 did not. Incidence of myocardial infarction was lower in the treated cohort than in the untreated cohort (1.2% vs 2.6%; P = 0.03). However, it remains unclear whether the event preceded the treatment, and incomparability in natural history or extraneous determinants was not taken into account in the analysis. The second study investigated 501 patients with gout prescribed colchicine and an equal number of matched patients who did not receive therapy. 31 Incidence rates of myocardial infarction, stroke, or transient ischemic attacks per 1000 person-years were 35.6 for users of colchicine and 81.8 for nonusers of colchicine, corresponding to a 49% lower risk (hazard ratio [HR], 0.51; 95% CI, 0.30–0.88) after adjustment for confounding factors. For all-cause mortality, a 73% reduction was observed (adjustedHR, 0.27; 95%CI, 0.17–0.43). Risk for residual confounding by indication remains high in such studies, but they still serve well as hypothesis- generating research.