Aggregates of endothelial microparticles and platelets circulate in peripheral blood. Variations during stable coronary disease and acute myocardial infarction.

Introduction: Activated endothelial cells on the surface of atherosclerotic plaques can shed membrane microparticles (MPs) with procoagulant potential. We have investigated whether circulating endothelial MPs could bind platelets, form aggregates, and be involved in thrombus formation during acute myocardial infarction (AMI).

Patients/methods And Results: We first assessed the in vitro formation of aggregates comprising endothelial MPs and platelets by incubating supernatants of activated endothelial cells in culture with freshly isolated platelets. Endothelial MP-platelets (EMP-P) aggregates were characterized by flow cytometry using antibodies to specific markers of endothelial cells and of platelets. Identical EMP-P aggregates were detected in vivo in the peripheral blood of healthy individuals, of patients with stable coronary disease (SCD), and of patients with AMI. The levels of EMP-P aggregates were significantly higher in patients with SCD than in controls (16.7+/-1.8/microl versus 7.1+/-0.3/microl, P<0.0002). In contrast, the levels of EMP-P aggregates in the first hours of AMI were significantly lower than in controls and in SCD, both before primary angioplasty (2.5+/-0.7/microl) and 2 h after reperfusion (1.7+/-0.3 microl) (P<0.0001 versus healthy controls and versus SCD). However, 48 h after the onset of AMI, the levels of EMP-P aggregates (14.7+/-1.8/microl) had returned to values close to those observed in SCD.

Conclusions: Endothelial MPs can bind to platelets and form aggregates. The enumeration of those aggregates in peripheral blood shows significant differences between the various groups of patients tested. This new test can help in the evaluation of the level of endothelial cell activation and the damages created by chronic atherosclerosis.