Atherosclerosis is an inflammatory arterial disease, which is the leading cause of several cardiovascular diseases. Elevated serum amyloid A (SAA), a positive acute-phase reactant, predicts future acute cardiovascular events and is associated with increased progression of atherosclerosis and endothelial dysfunction. Endothelial microvesicles are biomarkers of endothelial dysfunction in cardiovascular diseases and accumulate in atherosclerotic lesions. The aim of our study was to investigate the influence of SAA on microvesicle release in endothelial cells. Because microvesicles are known to participate in inflammation and coagulation, we determined, whether endothelial microvesicles could reflect SAA-induced proinflammatory and procoagulant response in endothelial cells. Since serum levels of anti-SAA antibodies are significantly lower in arterial thrombosis and some autoimmune diseases with accelerated atherosclerosis than in healthy blood donors, we investigated the influence of anti-SAA antibodies on endothelial microvesicle release. Human coronary artery endothelial cells were stimulated with human recombinant SAA and microvesicles were isolated by differential centrifugation following different times of stimulation. Flow cytometry was used to measure endothelial microvesicle number, annexin A5 binding and CD31, CD62E and tissue factor exposure. The inflammatory response was measured using interleukin-6 and interleukin-8 protein levels and the procoagulant response was measured with tissue factor exposure and activity. We demonstrated that SAA stimulation causes microvesicle release from endothelial cells. A time-dependent rise in microvesicle number correlated with interleukin-6 end interleukin-8 levels. The number of annexin A5, CD31 and CD62E-positive microvesicles (elevated in different cardiovascular diseases, such as coronary artery disease) increased with the time of stimulation. SAA caused tissue factor expression on microvesicles to peak at 4 hours and this increase correlated with tissue factor expression and activity in endothelial cells. Altogether, we showed that SAA causes microvesiculation that reflects inflammatory and procoagulant responses in endothelial cells. Anti-SAA antibodies decreased SAA-induced microvesicle release following 4 hour and 24 hour stimulation. Endothelial microvesicles may serve as biomarkers and/or mediators of SAA-induced changes of endothelial function.