title: Serum concentration of NSE and S-100b during LVAD in non-resuscitated patients.
abstract: OBJECTIVE
  Increased serum concentrations of brain-derived proteins neuron-specific enolase (NSE) and protein S-100beta (S-100b) are used as early predictors of long-term outcome in unconscious survivors after cardiopulmonary resuscitation (CPR). We investigated whether use of short-term Left Ventricular Assist Devices (LVAD) in patients undergoing percutaneous coronary intervention (PCI) effect serum concentrations of NSE and S-100b, because use of such devices in resuscitated cardiogenic shock patients increased during the last years.
  
  
  METHODS
  We analysed data from 80 consecutive non-resuscitated patients who received LVAD support. 43 patients with uncomplicated myocardial infarction (AMI) without LVAD support after PCI formed the reference group.
  
  
  RESULTS
  69 patients (86%) with LVAD support survived and were discharged from hospital. We observed an increase in NSE serum levels in 93.6% and in S-100b serum levels in 58.6% of these patients during LVAD support. This increase was significant in comparison to the upper limit of normal (ULN) of both biomarkers and to the reference group. Cardiogenic shock patients showed significantly higher serum concentrations of both neuroproteins than patients after high-risk PCI, and after AMI during LVAD support. The use of axial flow pumps led to significantly higher serum concentrations of NSE compared to patients on IABP, but not of S-100b. Thrombocytes and haemoglobin (Hb) concentrations declined significantly during LVAD support. Surprisingly, we also observed a significant increase in NSE in the reference group.
  
  
  CONCLUSIONS
  LVAD support after PCI is associated with a significant increase in NSE serum concentration as well as in S-100b. We therefore postulate an overestimation of the extent of hypoxic brain damage in unconscious survivors after CPR if treatment include LVAD support or PCI or both procedures. The increase in NSE can be partly explained by alteration of thrombocytes and other blood cells. However, the increase in S-100b remains unexplained since S-100b does not occur in peripheral blood cells. An additional release of both biomarkers from ischemic myocardium or cerebral microembolism should be drawn into consideration.
authors.affiliation: Department of Internal Medicine I, Division of Cardiology and Intensive Care Medicine, University of Jena, Jena, Germany. Ruediger.Pfeifer@med.uni-jena.de
authors.forename: Rüdiger
authors.initials: R
authors.lastname: Pfeifer
authors.forename: Markus
authors.initials: M
authors.lastname: Ferrari
authors.forename: Angelika
authors.initials: A
authors.lastname: Börner
authors.forename: Thomas
authors.initials: T
authors.lastname: Deufel
authors.forename: Hans R
authors.initials: HR
authors.lastname: Figulla
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000704:Analysis of Variance; D015415:Biomarkers / Q000097:blood; D005260:Female; D006353:Heart-Assist Devices; D006801:Humans; D008297:Male; D008875:Middle Aged; D010751:Phosphopyruvate Hydratase / Q000097:blood*; D011237:Predictive Value of Tests; D009418:S100 Proteins / Q000097:blood*; D012770:Shock, Cardiogenic / Q000097:blood* / Q000628:therapy*; D018709:Statistics, Nonparametric
chemical_list: D015415:Biomarkers; D009418:S100 Proteins; D010751:Phosphopyruvate Hydratase