Increasing evidence shows that inflammatory mediators play a pathogenic role in atherogenesis and acute coronary syndrome.1 In particular, several reports suggest that inflammatory cytokines such as tumour necrosis factor α (TNFα), interleukin (IL)-1 and various chemokines (for example, IL-8) may enhance degradation of the connective tissue matrix protein by activating matrix metalloproteinases (MMPs) and induce apoptosis of cells within the atherosclerotic lesion, promoting plaque destabilisation and rupture.1 2 These findings indicate a pathogenic link between persistent immune activation and plaque rupture in coronary artery disease. It is well established that platelets also contribute to the pathogenesis of acute coronary syndromes by promoting thrombus formation. However, recent studies suggest that these cells also may trigger an acute coronary event through other mechanisms, such as stimulation of an inflammatory response within the atherosclerotic plaque.