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Original Articles: Adult Cardiac

Cellular Immunity Impaired Among Patients on Left Ventricular Assist Device for 6 Months

Department of Surgery, Virginia Commonwealth University Hospitals, Richmond, Virginia

Accepted for publication January 17, 2008.

^_* Address correspondence to Dr Kimball, Box 980005, Virginia Commonwealth University Hospitals, Richmond, VA 23298 (Email: pkimball{at}gems.vcu.edu).

Background: Sustained maintenance on left ventricular assist device (LVAD) is associated with an increased frequency of severe infections. Although temporary changes in cellular immunity are seen immediately after implantation, the consequence of sustained LVAD treatment on immunity is unknown.

Methods: In vitro functional and phenotypic markers of T cell activation and 6 month clinical outcome were compared between patients with 6-month LVAD therapy and heart failure control patients.

Results: Recipients of LVADs had more infections (45.5% versus 0%; p < 0.05) and mortality (54% versus 16%; p < 0.05) than control patients. T-cell proliferative responses were lower among LVAD recipients than control patients when challenged with phytohemagglutinin (3.4 ± 4.7 versus 28.5 ± 19.6; p < 0.01), anti-CD3 (4.3 ± 4.5 versus 16.4 ± 17; p < 0.01), and staphylococcal enterotoxin B (7.2 ± 6.3 versus 26.1 ± 15.6; p = 0.002). Proliferative hyporesponsiveness among LVAD recipients was not caused by apoptosis (2.6% ± 2.7% versus 2.7% ± 2.1%; p = 0.94) or insufficient CD4+ cells (42.1% ± 11.3% versus 40.2% ± 7.5%; p = 0.71) relative to control patients. Instead, CD3+ cells from LVAD patients expressed less interleukin 2 (2.5% ± 1.5% versus 5.2% ± 3.1%; p = 0.03) and tumor necrosis factor- (6.0% ± 3.5% versus 25.8% ± 8.7%; p < 0.001) and more interleukin 10 (5.8% ± 6.1% versus 2.6% ± 2.1%; p < 0.05). In addition, suppressive T-regulatory cells were more prevalent in LVAD patients than control patients (12.9% ± 3.2% versus 1.2% ± 1.1%; p < 0.001).

Conclusions: Cellular immunity is compromised among long-term LVAD recipients because of a downregulatory cytokine imbalance and emergence of suppressive T-regulatory cells.

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