The Role of Colchicine in Acute Coronary Syndromes

Abstract

Despite promising results in small prospective observational and randomized trials, there is a need for more evidence evaluating the role of colchicine as a secondary preventive agent after ACSs.

Why Colchicine Should Be Considered for Secondary Prevention of Atherosclerosis: An Overview

“…46 (A detailed assessment of this evidence is presented in this issue. 47,48 ) Of relevance in patients with cardiovascular disease, colchicine 0.5 mg/d does not affect lipid levels, bleeding time, or blood pressure; it is not proarrhythmic; and it has never been reported to cause any clinically important drug interaction when prescribed with the full range of medications commonly used in the treatment of cardiovascular disease. Of the potential drug interactions between colchicine and drugs eliminated via hepatic cytochrome P-450 isozyme 3A4, only the interaction with clarithromycin appears clinically important, and only when colchicine is administered at a dose of >1 mg/d.…”

Colchicine-Binding Site Inhibitors from Chemistry to Clinic: A Review

“…It is also used to treat familial Mediterranean fever [11], Bechet's disease [12] and recurring pericarditis with effusion. Experimental medical use includes treatment of acute coronary syndromes [13]. This utilises colchicine's inhibition of a nucleotide-binding domain (NOD)-like receptor protein 3 (NLRP3) inflammasome protein complex, a novel pathway independent of colchicine's effects as an MTA.…”

“…Maguire and co-workers utilized the dihydronapthalene molecular scaffold (highlighted in blue, Figure 6) to synthesise two CA-4 derivatives KGP03 (26, Figure 6) and KG413 (27, Figure 6) as promising inhibitors of tubulin polymerisation. Their work was based on prior investigation of Oxi8006 (28, Figure 6), an indole derivative [80] and phenstatin (13) [58,81]. Compounds 26 and 27 were found to have IC 50 values for the inhibition of tubulin polymerisation of 0.46 and 0.85 µM, akin to CA-4 (IC 50 = 1.2 µM).…”

Acute coronary syndrome: how to reduce the residual inflammatory risk?

“…Механизм дей ствия колхицина окончательно неизвестен, обсуждается несколько возможных точек приложения, приводящих к снижению активности NLRP3 инфламмасом и синтеза провоспалительных цитокинов. Применение колхицина у больных ИБС и влияние на активность маркеров воспаления ранее изучалось в нескольких небольших исследованиях, давших противоречивые результаты [43]. В ноябре 2019г были представлены результаты первого крупного многоцентрового исследования по эффективности колхицина у больных, перенесших ОКС [44].…”