The Canakinumab Antiinflammatory Thrombosis Outcome Study trial—the starting gun has fired

David Crossman, Alexander Rothman


When teaching clinical undergraduates about the cause of atherosclerosis the lecturer will highlight risk factors such as smoking, hypercholesterolaemia and hypertension that are mutable for therapeutic benefit. If the same lecturer were to be talking to their science laboratory staff they would discuss inflammatory paradigms in the vessel wall that lead to lipid accumulation in monocyte-derived macrophages that become foam cells. Depending upon the local plaque microenvironment and T cell repertoire these monocyte-derived macrophages direct either plaque stability and/or resolution of inflammation through production of smooth muscle cell mitogens or release proinflammatory cytokines, matrix metalloproteinases and express tissue factor that promotes a disorganised, thrombogenic plaque with lesion progression and associated myocardial infarction or stroke (1). A bright student might ask whether the inflammatory process can be altered for therapeutic benefit? Until the recent publication of the Canakinumab Antiinflammatory Thrombosis Outcome Study (CANTOS) trial the answer would have been, no. So, has CANTOS really changed the response to, yes?