Quantitative changes in T-cell populations after left ventricular assist device implantation: relationship to T-cell apoptosis and soluble CD95.
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.
Ankersmit
H J
HJ
College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA.
Edwards
N M
NM
Schuster
M
M
John
R
R
Kocher
A
A
Rose
E A
EA
Oz
M
M
Itescu
S
S
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
D019014:fas Receptor