Endothelial cells (ECs) have long been implicated in the pathogenesis of various clinical disorders such as thrombosis, inflammation, and vascular diseases (1,2). However our knowledge of precisely how ECs contribute to the pathogenesis of human disease remains limited. A major obstacle to the study of endothelial disturbances is the difficulty in sampling ECs from patients for investigation. Clinical tests to assess or monitor EC perturbations are not widely available, yet there is an urgent need for diagnostic assays that are clinically useful, simple, and economical. The availability of such methods promises new insights into the role of ECs in the pathogenesis of vascular disorders and will assist clinicians in the early diagnosis and prevention of common atherothrombotic conditions, the leading cause of mortality in our hemisphere.

This situation has improved in the last few years, as it has become evident that ECs, like other blood cells, shed membranous vesicles, termed endothelial microparticles (EMPs), in amounts and phenotypes that reflect the health of the parent cell. EMP assays offer a new and sensitive means of assessing endothelial status (3).

ECs normally present a nonadhesive and anticoagulant surface to flowing blood, but EC injury can provoke cell adhesion and initiation of coagulation with consequent thrombosis and inflammation (1, 4). EMPs consist of somewhat heterogeneous species of microparticles (<1 μm diameter) carrying many biomarkers of the parent cells, the analysis of which can therefore provide useful information about EC status (3). For example, it has been shown that EMPs released upon activation exhibit distinctive antigenic phenotypes and functional properties compared to those released upon apoptosis (5).