Inflammation is deeply involved in the pathophysiology of ischemia- reperfusion (I/R) lesions and remodeling phenomena after an acute myocardial infarction (AMI), responsible for heart failure. Colchicine exerts antiinflammatory effects, through the inhibition of neutrophil chemoattraction, the inflammasome and proinflammatory cytokines. We aimed at evaluating the impact of colchicine on the infarct size in a mouse model.

Myocardial I/R injury were induced in 19, 8 to 10 weeks, male C57BL/6 mice, after left thoracotomy, by ligating the left coronary artery for 45 min followed by reperfusion. 400 μg/kg of Colchicine or placebo was administrated via the intraperitoneal (i.p) route 25 minutes before the reperfusion (blinded administration). 24 hours later, mice were sacrificed after intracardiac Evans blue injection, the heart was removed and the left ventricle (LV) was cut in transverse slices stained with Triphenyl-tetrazolium chloride (TTC). The area at risk (AAR) and infarcted area (IA) were determined by computerized planimetry, the AAR/total area and IA/AAR ratios were calculated. All data are expressed as percentage mean and standard error of mean.

10 animals were included in the control group and 9 in the Colchicine group (blinded adjudication). All the animals were successfully operated and survived at 24 hours. The AAR/total area ratios were respectively 54.44 ±2.9% in the Colchicine group versus 51.96 ±4.4% in the control group, p= n.s. No difference in infarct size could be found in Colchicine treated mice in comparison to control mice with IA/AAR ratios respectively at 49 ±3.4% versus 53.7 ±5.3%, p= n.s.

In conclusion, reduction of infarct size could not be obtained by treatment with Colchicine at the present concentration after induced myocardial infarction in mice. Further analysis should be performed to evaluate inflammatory cells accumulation in myocardium and inflammation pathways as well as LV remodeling.

The author hereby declares no conflict of interest