The incidence of diabetes is increasing in the general population because of increasing obesity, and is likely to result in a higher incidence of coronary artery disease. It was recently reported that diabetics (types I and 11) dying suddenly from coronary artery disease have greater macrophage and T lymphocyte infiltration in atherosclerotic plaques, as well as larger necrotic cores compared with nondiabetics. The inflammatory cell infiltrates showed human leukocyte antigen-DR expression, which was greater in diabetics. The receptors for advanced glycosylation end-products expression, demonstrated by immunohistochemistry, was greater in diabetics than in nondiabetics in macrophages, smooth muscle cells and endothelial cells, and was associated with apoptosis of macrophages and smooth muscle cells, but not of endothelial cells. There is also a higher incidence of healed plaque ruptures and healed myocardial infarct in type II diabetics. Plaque burden is higher in diabetics than in ondiabetics; however, distal plaque burden was only significantly different in type II diabetics compared with nondiabetics. There was greater positive remodelling in diabetic coronary arteries than in nondiabetic ones, which correlated with the per cent necrotic core. Further studies are needed to better understand the mechanisms that govern greater inflammation and plaque burden in diabetics.