The contribution of platelets to the pathogenesis and progression of vascular complications in diabetes is supported by several studies. In general, platelets obtained from diabetic subjects show increased adhesiveness and an exaggerated aggregation, both spontaneous and in response to stimulating agents. The causes for this activation are multifold: altered exposure and/or abundance of glycoprotein receptors for agonists and adhesive proteins on the platelet surface, increased binding of fibrinogen, decreased membrane fluidity, altered platelet metabolism and changes in intraplatelet signalling pathways. The altered biophysical state of platelet membrane components in diabetes mellitus may be one of the major determinants of platelet hypersensitivity and hyperfunction and may contribute to impairments in various metabolic pathways, like intensified calcium mobilisation and accentuated thromboxane synthesis and release. Activated platelets interact with other cells, such as endothelial cells and leukocytes as well with the coagulation system in the process of atherosclerosis. Some studies indicated that platelet dysfunction was especially apparent in diabetic subjects with macro- or microangiopathy, while others showed that it may be related to the presence of diabetes mellitus per se. Several pharmaceutical compounds have been developed for the inhibition of platelet activation. However, aspirin treatment is cheap and effective, and aspirin remains to be the drug of choice for diabetic patients. It should be prescribed widely for patients who are at high risk of cardiovascular events.