Usefulness of cell-mediated immune function in risk stratification for patients with advanced heart failure - 18/04/17
Background |
Although heightened inflammation and autoimmune responses have been well described in patients with heart failure, the role of cell-mediated immune function in the pathogenesis and progression of heart failure is unclear. The aim of our study is to evaluate the prognostic role of cell-mediated immune function in patients with advanced heart failure.
Methods |
We studied patients with advanced heart failure referred for evaluation of candidacy for advanced heart failure therapies between 2007 and 2010. Cell-mediated immune response was categorized into 3 groups—low or poor immune response (≤225 ng/mL), moderate or normal immune response (226-524 ng/mL), and strong immune response (≥525 ng/mL)—using a phytohemagglutinin-stimulated T-cell response assay.
Results |
Out of 368 patients, 41 patients (11.1%) had poor immune function, 258 patients (70.1%) had normal immune function, and 69 patients (18.7%) had strong immune function. The primary outcome of all-cause mortality or cardiac transplantation occurred in 63.4%, 45.3%, and 34.8% in the poor immunity, normal immunity, and strong immune function groups, respectively. In univariate analysis, cell-mediated immune function was strongly associated with the primary outcome (P=.014). Poor immune function portended worse prognosis (hazard ratio=2.18, 95% CI 1.01-4.70, P=.047), and strong immune function was associated with better survival (hazard ratio=0.67, 95% CI 0.43-1.04). However, when adjusted for multiple variables in multivariate analysis, immune function status lost its overall significance to predict primary outcome (P=.11), but the direction to an increased risk of primary outcome was maintained in the poor immune function group.
Conclusions |
Poor cell-mediated immune function measured by a clinically available assay could be associated with more adverse long-term prognosis in patients with advanced heart failure.
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Funding support: There is no extramural funding for this project. Dr Tang is funded by grants from National Institutes of Health (RO1 HL103931). |
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Conflict of interest disclosure: All authors have no relationships to disclose. All authors have approved the final draft of the manuscript. |
Vol 183
P. 35-39 - janvier 2017 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
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