Journal
CLINICAL RESEARCH IN CARDIOLOGY
Volume 108, Issue 2, Pages 133-141Publisher
SPRINGER HEIDELBERG
DOI: 10.1007/s00392-018-1331-2
Keywords
Leukocyte; Monocyte; Macrophage; T cell; Heart failure; Prognosis
Categories
Ask authors/readers for more resources
BackgroundActivated leukocytes may contribute to the development and progression of heart failure (HF). We investigated the predictive value of circulating levels of stable and readily detectable markers reflecting both monocyte/macrophage and T-cell activity, on clinical outcomes in HF patients with reduced ejection fraction (HFrEF).MethodsThe association between baseline plasma levels of soluble CD163 (sCD163), macrophage migration inhibitory factor (MIF), granulysin, soluble interleukin-2 receptor (sIL-2R), and activated leukocyte cell adhesion molecule (ALCAM) and the primary endpoint of death from any cause or first hospitalization for worsening of HF was evaluated using multivariable Cox proportional hazard models in 1541 patients with systolic HF and mild to moderate anemia, enrolled in the Reduction of Events by darbepoetin alfa in Heart Failure (RED-HF) trial. Modifying effects and interaction with darbepoetin alfa treatment were also assessed.ResultsAll leukocyte markers, except granulysin, were associated with the primary outcome and all-cause death in univariate analysis (all p<0.01) and remained significantly associated in multivariable analysis adjusting for conventional clinical variables (e.g. age, gender, BMI, NYHA class, creatinine, LVEF, etiology) and CRP. However, after final adjustment for TnT and NT-proBNP no associations were found with outcomes. No interaction with darbepoetin alpha treatment was observed for any marker.ConclusionsLeukocyte activation markers sCD163, MIF, sIL-2R, and ALCAM were associated with adverse outcome in patients with HFrEF, but add little as prognostic markers on top of established biochemical risk markers.Clinical Trial Registrationhttps://clinicaltrials.gov/ct2/show/NCT00358215.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available