Phenotypic assessment of endothelial microparticles in patients with heart failure and after heart transplantation:: Switch from cell activation to apoptosis

Background: Endothelial microparticles (EMPs) are sub-microscopic membrane vesicles that are shed from the surface of endothelial cells during activation, injury and/or apoptosis. Endothelial cells release phenotypically and quantitatively distinct endothelial microparticles (EMPs) in activation and apoptosis. Therefore, the phenotypic assessment of EMPs can provide useful information reflecting the nature of endothelial injury. We tested the hypothesis that heart transplantation (HT) modifies the pattern of endothelial injury seen in patients with congestive heart failure (CHF). Methods: Flow cytometry was used to measure EMPs identified by E-selectin (CD62) and platelet-endothelial cell adhesion molecule 1 (CD31) in 23 patients with advanced heart failure and in 23 HT recipients. A cohort of 23 healthy individuals served as controls. Results: Heart failure patients were found to have significantly higher levels of EMP62E (577 counts/mu l) than controls (192 counts/mu l) and post-transplant patients (152 counts/mu l) (p < 0.0001). Levels. of endothelial microparticles expressing CD31 were significantly different among study groups (analysis of variance [ANOVA], p = 0.001). Heart failure patients had significantly higher levels (1,526 counts/mu l) than controls (395 counts/mu l) (p < 0.01). Levels of EMP31 remained elevated after heart transplant (935 counts/mu l) (p = non-significant). The EMP62/EMP31 ratio, an index of activation (high ratio) or apoptosis (low ratio), was significantly different between the groups (ANOVA, p = 0.01). Post-transplant patients had significantly lower ratios (0.16) than CHF patients (0.38) and controls (0.49). Conclusions: Cardiac transplantation is associated with a different pattern of endothelial cell injury than that seen in heart failure. The phenotypic assessment of EMPs in post-transplant patients is consistent with increased apoptotic activity.