Colchicine for Coronary Artery Disease: A Review

Abstract

Coronary artery disease is a serious threat to human health. More and more evidences indicate chronic inflammatory plays a key role in the development of this disease. Inflammation markers are gradually used in the diagnosis and treatment. Although the treatment of coronary heart disease with colchicine is still controversial, more and more studies showed that patients can benefit from this medicine. In this review, we discuss and summarize colchicine on essential pharmacology, anti-inflammatory mechanism of action, and the most important and recent clinical studies. According to these literatures, colchicine possibly will possibly become a new valuable and cheap medicine for the treatment of coronary artery disease.

Frontiers and hotspots evolution in anti-inflammatory studies for coronary heart disease: A bibliometric analysis of 1990–2022

“…Colchicine is widely used in clinical practice for gout ( 113 , 134 , 135 ). The LoDoCo ( 136 ) study suggested that colchicine reduced the relative risk of the primary endpoint event (acute coronary syndrome, out-of-hospital cardiac arrest, or non-cardiogenic embolic ischemic stroke) by 67% in 532 patients with stable coronary artery disease treated with low-dose colchicine (0.5 mg/day) (HR, 0.33; 95% CI, 0.18 to 0.59; p < 0.001).…”

Study on the mechanism of action of colchicine in the treatment of coronary artery disease based on network pharmacology and molecular docking technology

“…Notably, it was reported that MPO can affect nitric oxide (NO) metabolism in the vascular endothelium by reducing NO production and inhibiting Bcl-2 expression, triggering apoptosis of endothelial cells and leading to vascular endothelial dysfunction ( Kimak et al, 2018 ). And colchicine promotes NO production and exerts a protective endothelial function, probably by inhibiting the MPO pathway ( Chen et al, 2022 ). Furthermore, it has been shown that MPO is also involved in the formation of neutrophil extracellular traps (NETs), which can activate the inflammatory response, promote the expression of MPO itself and its associated inflammatory factors, release matrix metalloproteinases and oxidants, and promote the formation, destabilization, as well as rupture of atherosclerotic plaques ( Borissoff et al, 2013 ; Döring et al, 2017 ).…”