Colchicine reduces ischemic events in CAD but causes GI upset: Study

Coronary artery disease is the buildup of plaque in the arteries that supply oxygen-rich blood to your heart. Plaque causes a narrowing or blockage that could result in a heart attack. Inflammation plays a crucial role in coronary artery disease (CAD). The anti‐inflammatory drug colchicine seems to reduce ischemic events in patients with coronary artery disease (CAD). However, not much data is available on its safety profile and impact on mortality.

A group of researchers from Switzerland conducted a systematic review and meta‐analysis to evaluate the utility of colchicine in patients with acute and chronic coronary artery disease (CAD).

The researchers searched MEDLINE, EMBASE, Cochrane CENTRAL, and conference abstracts from January 1975 to October 2020. Randomized trials assessing colchicine compared with placebo/standard therapy in patients with coronary artery disease (CAD) were included. Data were combined using random‐effects models. The reliability of the available data was tested using trial sequential analyses.

The results of the study are as follows:

• Of 3108 citations, 13 randomized trials (n=13,125) were included. Colchicine versus placebo/standard therapy in patients with CAD reduced risk of myocardial infarction and stroke/transient ischemic attack.
• But treatment with colchicine compared with placebo/standard therapy had no influence on all‐cause and cardiovascular mortality.
• Colchicine increased the risk for gastrointestinal side effects.
• According to trial sequential analyses, there is only sufficient evidence for a myocardial infarction risk reduction with colchicine.

The researchers concluded that among patients with CAD, colchicine reduces the risk of myocardial infarction and stroke, but has a higher rate of gastrointestinal upset with no influence on all‐cause mortality.

Reference:

A study titled, "Colchicine in Patients with Coronary Artery Disease: A Systematic Review and Meta‐Analysis of Randomized Trials" by Thomas Kofler published in the Journal of the American Heart Association.

DOI: https://doi.org/10.1161/JAHA.121.021198