A recent randomized controlled trial by Giannopoulos et al demonstrated the benefit from perioperative use of colchicine in patients undergoing elective coronary artery bypass grafting presumably through its anti-inflammatory properties. Maximal high-sensitivity troponin T concentration within 48 hours after the operation was significantly lower in the colchicine group than the placebo group. We were attracted to this interesting cleverly designed trial and the well-written report. However, we intended to point out potential confounders.

Colchicine is an old anti-inflammatory agent mostly prescribed for acute gout attacks, which are a manifestation of hyperuricemia. Colchicine neither takes part in uric acid metabolism nor lowers the serum uric acid level, but it might relieve acute inflammatory reaction associated with urate deposit through inhibition of neutrophil mobility and activity. Given that statins have well-known pleiotropic effects, including improvement of endothelial dysfunction, antioxidant properties, and inhibition of inflammatory responses, preoperative treatment with statins has been found to be associated with decreased postoperative complications including myocardial infarction. As a class I recommendation according to contemporary guidelines, the use of statins in this trial was suboptimal (73% in the colchicine group and 83% in the placebo group). It is unclear whether the anti-inflammatory effect of colchicine will be attenuated by more optimal statin use.

Hyperuricemia has been found to be correlated with a number of cardiovascular diseases. We have retrospectively analyzed all consecutive patients who presented with ST elevation myocardial infarction and underwent primary percutaneous coronary intervention at our hospital, a tertiary medical center in Taiwan, during a 5-year period. We found that in those with low risk who were classified as Killip class I (n = 507), hyperuricemia was independently associated with all-cause 1-year mortality (adjusted hazard ratio 5.418, 95% confidence interval 1.577 to 18.619). However, this correlation did not exist in patients with Killip II to IV classification. Our interpretation is that hyperuricemia represents one manifestation of systemic inflammation particularly important in patients with low disease severity. In the present trial by Giannopoulos et al, the EuroSCORE II of the colchicine and placebo groups was 2.21 ± 0.96% and 2.34 ± 0.99% (expressed as mean ± SD), respectively, which was relatively low in patients undergoing coronary artery bypass grafting in clinical practice. It could not be excluded that the beneficial effect of colchicine might be restricted to the low-risk group only. Therefore, disease severity (e.g., EuroSCORE II, Killip classification, TIMI risk score, and so on) should be considered as a potential confounder in subsequent clinical trials.