Low-Dose Colchicine for Secondary Prevention of Coronary Artery Disease: JACC Review Topic of the Week
- PMID: 37558377
- DOI: 10.1016/j.jacc.2023.05.055
Low-Dose Colchicine for Secondary Prevention of Coronary Artery Disease: JACC Review Topic of the Week
Abstract
Among statin-treated patients, inflammation assessed by means of high-sensitivity C-reactive protein (hsCRP) is a more powerful determinant of cardiovascular death and all-cause mortality than low-density-lipoprotein cholesterol (LDL-C). Several therapies that target residual inflammatory risk significantly reduce vascular event rates. For coronary artery disease patients already taking guideline-directed medical care, including statins, low-dose colchicine (0.5 mg/d orally) has been shown to safely lower major adverse cardiovascular events by 31% among those with stable atherosclerosis and by 23% after recent myocardial infarction. These magnitudes of benefit are larger than those seen in contemporary secondary prevention trials of adjunctive lipid-lowering agents. Low-dose colchicine is contraindicated in patients with significant renal or liver dysfunction and should be temporarily discontinued when taking concomitant agents such as clarithromycin, ketoconazole, and cyclosporine that share metabolism pathways. Lipid lowering and inflammation inhibition are not in conflict but are synergistic. In the future, combined use of aggressive LDL-C-lowering and inflammation-inhibiting therapies may become standard of care for most atherosclerosis patients. In June 2023, the U.S. Food and Drug Administration approved the use of low-dose colchicine to reduce the risk of myocardial infarction, stroke, coronary revascularization, and cardiovascular death in adult patients with established atherosclerotic disease or with multiple risk factors for cardiovascular disease.
Keywords: atherosclerosis; colchicine; inflammation; residual inflammatory risk.
Copyright © 2023 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
Conflict of interest statement
Funding Support and Author Disclosures Dr Ridker has received institutional research grant support from Kowa, Novartis, Amarin, Pfizer, Esperion, Novo Nordisk, and the National Heart, Lung, and Blood Institute; has served as a consultant to Novartis, Flame, Agepha, AstraZeneca, Janssen, Civi Biopharm, Glaxo Smith Kline, SOCAR, Novo Nordisk, Omeicos, Health Outlook, Montai Health, New Amsterdam, Boehringer Ingelheim, RTI, Zomagen, Cytokinetics, Horizon Therapeutics, and Cardio Therapeutics; has minority shareholder equity positions in Uppton, Bitteroot Bio, and Angiowave; and receives compensation for service on the Peter Munk Advisory Board (University of Toronto), the Leducq Foundation, Paris FR, and the Baim Institute (Boston). All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
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