Conceivable triggers for endothelial damage might be hypoxia [30] or shear stress [35,36]. Therefore, this site it seems possible that shear stress during mechanical chest compression or the action itself is another cause of enhanced detachment of CEC from the endothelial layer.We obtained comparatively high absolute values of CECs in this study, compared with the literature. In our opinion this indicates massive endothelial damage after CPR that largely exceeds the values detected in other diseases described so far in the available literature. This underlines the severity of this life-threatening condition, associated with complete discontinuation of circulation and high mortality. On the other hand, CEC counts in the literature vary from 15 to 670 cells/mL in various disease states [33,37], which points out the inhomogeneity of this relatively new method.

Furthermore, different methodical approaches might change the absolute values.Interestingly, and in contrast to the CECs, the number of EMPs in resuscitated patients rises further in the first 24 hours after ROSC, hence reflecting an ongoing process of endothelial damage. As EMPs are elevated in several systemic inflammatory diseases such as vasculitis [38] and sepsis [39], the noticeable increase in EMP numbers could be due to the systemic inflammatory response occurring after CPR maintaining endothelial injury. EMP may express adhesion molecules specific to mature endothelial cells, such as platelet-endothelial cell adhesion molecule-1 (CD31), VE-cadherin (CD144), or MCAM (CD146).

Activation of endothelial cells with TNF-�� induced the formation of EMPs [16] exposing adhesion-cell molecules, including E-selectin (CD62E) or intercellular adhesion molecule-1 (CD54). In this study, we measured activation-induced EMPs by detection of E-selectin-positive microparticles. A possible explanation for the ongoing endothelial injury in the post-resuscitation period could be ischemia and reperfusion during cardiac arrest and mechanical resuscitation.Interestingly, patients treated with statins prior to cardiac arrest showed slightly lower EMP counts. These results indicate a potential protective effect of statins on the endothelium during and after ischemia and reperfusion and encourage further investigation of the effect of statin treatment in post-resuscitation care.

Finally, in a smaller population, we were able to detect elevated numbers of EPC in patients on the second day after CPR as an indicator of the early onset of endothelial repair. EPC-mediated vascular repair has been shown to be associated with normalization of endothelial function and restoration of blood flow at the site of injury [21]. These circulating cells are capable of GSK-3 endothelial differentiation and homing to ischemic tissues [20].