Colchicine to prevent sympathetic denervation after acute myocardial infarction: the COLD-MI trial
Fabien Huet, Denis Mariano‐Goulart, Sylvain Aguilhon, Quentin Delbaere, Alain Lacampagne, Jérémy Fauconnier, Florence Leclercq, Jean‐Christophe Macia, Mariama Akodad, Nidal Jammoul, Fabrice Prunier, Nathan Mewton, Denis Angoulvant, Catherine Lozza, Sonia Soltani, Annabelle Rodier, Sylvie Grandemange, Anne‐Marie Dupuy, Jean‐Paul Cristol, Maïlis Amico, Nicolas Nagot, François Roubille
Abstract
Colchicine demonstrated to reduce neutrophil migration, myocardial necrosis,1 and myocardial denervation in the remote area in mice.2 In patients, colchicine reduced major cardiovascular events following acute myocardial infarction (AMI) in the Colchicine Cardiovascular Outcomes Trial (COLCOT),3 especially strokes. Sympathetic innervation is well-established to be particularly frail in cardiac tissue. The aim of this study was to explore the impact of colchicine on myocardial denervation following reperfused AMI patients by assessing the loss of presynaptic adrenaline reuptake function using 123I-metaiodobenzylguanidine single-photon emission computed tomography (123I-MIBG SPECT) imaging. The protocol has been described in detail elsewhere4. The COLD-MI trial was a single-centre, open-label, randomized controlled trial. Adult patients presenting a first episode of chest pain lasting <12 h and with a diagnosis of ST-elevation myocardial infarction (STEMI) and coronary occlusion on initial angiography were prospectively and consecutively included and randomized to receive either 1 mg colchicine tablets, one per day for 30 days, initiated within 48 h after revascularization or not (1:1 allocation ratio) for 30 days. Follow-up visit was performed at 1 and 6 months after randomization. The trial medication was provided by the in-hospital pharmacy (Figure 1).