Type 2 diabetes accounts for a large proportion of cardiovascular disease within the UK. Inflammation is increasingly seen as a core process (even touted as a causative factor) connecting the metabolic syndrome and cardiovascular disease. Inflammatory markers, adhesion molecules, transcription regulators such as PPAR-gamma and NF-kappa B are being recognised as key elements of the underlying pathological process. In particular the links between oxidative stress, metabolic syndrome components and a pro-inflammatory milieu are becoming increasingly recognised. Salicylates have been used extensively for more than a hundred years but remain the subject of much research and scientific debate. Mechanisms of aspirin action, such as effects on endothelial function, oxidative stress, hyperglycaemia, inflammation, and mechanisms of aspirin resistance are being elucidated. With the advent of COX-2 selective inhibitors, the importance of the cyclo-oxygenase (COX-1 & COX-2 enzymes) pathways and the implications of more selective COX manipulation are being re-evaluated. There is no universal consensus on the use and dose of aspirin in diabetes. This review focuses upon the impact that aspirin may have to ameliorate the pathophysiology of diabetes and CVD.