Abstract
Atherosclerotic cardiovascular disease is a leading cause of death and morbidity globally. Over the past several years, arterial inflammation has been implicated in the pathophysiology of athero-thrombosis, substantially confirming what pathologist Rudolf Virchow had observed in the 19th century. Lipid lowering, lifestyle changes, and modification of other risk factors have reduced cardiovascular complications of athero-thrombosis, but a substantial residual risk remains. In view of the pathogenic role of inflammation in athero-thrombosis, directly targeting inflammation has emerged as an additional potential therapeutic option; and some early promising results have been suggested by the Canakinumab Anti-inflammatory Thrombosis Outcome Study (CANTOS), in which canakinumab, a fully human monoclonal antibody targeting the pro-inflammatory and pro-atherogenic cytokine interleukin 1 beta, was shown to reduce cardiovascular events.