[Ten questions on colchicine as a "new" cardiovascular drug]

Colchicine is one of the more ancient drugs of vegetal origin still in use in clinical practice. It has been used for centuries as drug to treat gout, but its anti-inflammatory effects made it efficacious also in different cardiovascular indications (e.g. pericarditis, acute and chronic coronary syndromes, atrial fibrillation), that are well beyond its original indication. The treatment and prevention of pericarditis is the only registered cardiovascular indication in Italy (allowing prescription in class A by the National Healthcare System), while other indications are off-label. When used at low doses (0.5 mg/day), the drug is safe and efficacious with limited side effects, mainly gastrointestinal. Gastrointestinal absorption is fast since the drug is a small lipophilic molecule that is eliminated by cells through P-glycoprotein. Colchicine is metabolized by cytochrome P450 in the liver and mainly excreted into the biliary tract. It is also excreted, essentially unmodified, by the kidneys. It is concentrated in white blood cells, especially neutrophils, that are without P-glycoprotein. In these cells, blocking tubulin polymerization, colchicine reduces their function, also interfering with endothelial adhesion and platelet interactions. Moreover, it is responsible for a non-specific inhibition of the inflammasome, thus reducing the generation of pro-inflammatory cytokines, such as interleukin-1. The aim of this paper is to provide concise replies to the most common clinical questions on the use of colchicine for cardiovascular indications.