Vascular dysfunction is key to the development of thrombosis in the antiphospholipid syndrome. This has been largely demonstrated by the upregulation of various cell surface and intracellular signalling molecules, as well as proinflammatory cytokine release from activated endothelial cells. Endothelial microparticles (EMP) are a further marker of endothelial activation but have been less extensively studied. We summarise evidence suggesting that these microparticles may be critical effectors of thrombosis in the antiphospholipid syndrome. There is evidence that levels of EMP are raised in patients with circulating antiphospholipid antibodies and that these EMP may be prothrombotic. The balance between markers of endothelial dysfunction (including EMP and circulating endothelial cells) and markers of repair such as circulating endothelial progenitor cells may be abnormal in patients with APS but this has not been proved and requires further study.