title: Quantitative changes in T-cell populations after left ventricular assist device implantation: relationship to T-cell apoptosis and soluble CD95.
abstract: BACKGROUND
  Left ventricular assist devices (LVADs) are currently being evaluated as permanent therapy for end-stage heart failure. Because life-threatening infections limit successful long-term device implantation, we investigated the relationship between quantitative T-cell defects in LVAD recipients and CD95-mediated T-cell apoptosis.
  
  
  RESULTS
  Immunological studies were performed in NYHA class IV patients awaiting cardiac transplantation who received either a TCI Heartmate left ventricular assist device (LVAD) or medical management. Fluorochrome-labeled Mabs were used in T-cell phenotypic analyses. T-cell apoptosis was measured by annexin V binding of T cells cultured in medium for 24 hours. Circulating serum levels of soluble CD95 were measured by ELISA. LVAD recipients had a relative lymphopenia and reduction in CD4 T-cell levels compared with NYHA class IV heart failure controls. These observations were confirmed in a longitudinal study in LVAD recipients, which showed that device implantation was accompanied by progressive and sustained reductions in circulating CD4 T-cell levels. These abnormalities in LVAD recipients were accompanied by increased levels of circulating soluble CD95 and by excessive CD4 and CD8 T-cell apoptosis. Susceptibility to induction of apoptosis was >2-fold greater for CD4 T cells than for CD8 T cells.
  
  
  CONCLUSIONS
  These results suggest that the reduction in CD4 T-cell levels accompanying LVAD implantation is a consequence of an augmented pathway of CD95-mediated apoptosis. The clinical consequences of these abnormalities may include increased prevalence of systemic infections.
authors.affiliation: College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA.
authors.forename: H J
authors.initials: HJ
authors.lastname: Ankersmit
authors.forename: N M
authors.initials: NM
authors.lastname: Edwards
authors.forename: M
authors.initials: M
authors.lastname: Schuster
authors.forename: R
authors.initials: R
authors.lastname: John
authors.forename: A
authors.initials: A
authors.lastname: Kocher
authors.forename: E A
authors.initials: EA
authors.lastname: Rose
authors.forename: M
authors.initials: M
authors.lastname: Oz
authors.forename: S
authors.initials: S
authors.lastname: Itescu
mesh_terms: D017209:Apoptosis / Q000276:immunology; D003430:Cross-Sectional Studies; D006333:Heart Failure / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology / Q000628:therapy*; D006352:Heart Ventricles / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology; D006353:Heart-Assist Devices / Q000009:adverse effects; D006801:Humans; D016176:T-Lymphocyte Subsets / Q000276:immunology* / Q000473:pathology; D016277:Ventricular Function, Left; D019014:fas Receptor / Q000276:immunology
chemical_list: D019014:fas Receptor