title: Left ventricular assist system support is associated with persistent inflammation and temporary immunosuppression.
abstract: BACKGROUND
  In patients undergoing left-ventricular assist system support, it has not been elucidated to which extent mechanical circulatory support itself as opposed to the underlying condition of endstage heart-failure contributes to perturbation of immune homeostasis.
  
  
  METHODS
  In eleven heart transplant candidates who had to undergo Novacor left-ventricular assist device bridging, we prospectively sampled interleukin-6, T-cell and monocyte subsets and compared them to fifteen UNOS status II patients awaiting cardiac transplantation on medical heart failure treatment as outpatients at the time of LVAS implantation/listing decision as well as 2.0+/-1.2 months and 4.5+/-2.3 months later. In order to assess deviations in both groups from normal values, thirty-two healthy subjects served as reference group.
  
  
  RESULTS
  Patients undergoing Novacor bridging had higher C-reactive protein, leukocyte, neutrophil, and monocyte levels at all three times, and exhibited lower CD3 +, CD4+, CD3+/CD45 RO T-cell and natural killer cell counts than medically treated patients awaiting transplantation 2 months after the LVAS implantation/listing decision. In comparison to controls, both groups had higher levels of inflammatory activation and lower levels of immunocompetence at all three times.
  
  
  CONCLUSIONS
  While both groups of endstage heart failure patients show immunological alterations compared to controls, patients who have to be bridged by the Novacor LVAS exhibit a more pronounced activation of inflammatory markers. This may be due to more advanced heart failure but the device itself also may contribute to more pronounced inflammation and a temporary suppression of immunocompetent cells.
authors.affiliation: Department of Cardiothoracic Surgery, Münster University Hospital, Germany.
authors.forename: M C
authors.initials: MC
authors.lastname: Deng
authors.forename: M
authors.initials: M
authors.lastname: Erren
authors.forename: T D
authors.initials: TD
authors.lastname: Tjan
authors.forename: N
authors.initials: N
authors.lastname: Tamminga
authors.forename: B
authors.initials: B
authors.lastname: Werntze
authors.forename: P
authors.initials: P
authors.lastname: Zimmermann
authors.forename: M
authors.initials: M
authors.lastname: Weyand
authors.forename: D
authors.initials: D
authors.lastname: Hammel
authors.forename: C
authors.initials: C
authors.lastname: Schmidt
authors.forename: H H
authors.initials: HH
authors.lastname: Scheld
mesh_terms: D000328:Adult; D016022:Case-Control Studies; D005260:Female; D006333:Heart Failure / Q000276:immunology / Q000628:therapy*; D016027:Heart Transplantation; D006353:Heart-Assist Devices / Q000009:adverse effects*; D006801:Humans; D007121:Immunocompetence; D007249:Inflammation; D015850:Interleukin-6 / Q000032:analysis; D008297:Male; D008875:Middle Aged; D009000:Monocytes; D011446:Prospective Studies; D016176:T-Lymphocyte Subsets; D013997:Time Factors
chemical_list: D015850:Interleukin-6