Activation of lymphocyte autophagy/apoptosis mirror reflects hemodynamic inefficiency and functional aerobic impairment in patients with heart failure (706.19)

Abstract

This study investigated whether lymphocytopenia results from activated lymphocyte autophagy/apoptosis, which reflects hemodynamic inefficiency and functional aerobic impairment in patients with heart failure (HF). One hundred twenty‐seven HF patients were divided into the HF with non‐, mild‐, and severe‐lymphocytopenia groups. Lymphocyte autophagy/apoptosis and ventilatory/hemodynamic efficiencies were analyzed in these HF patients and 35 normal counterparts. The results showed that HF patients with severe lymphocytopenia revealed (i) more G protein‐coupled receptor kinase‐2 level, (ii) lesser mTOR level with higher LAMP‐2 expression and acridine orange staining, (iii) lower mitochondrial transmembrane potential with higher caspase‐3 activation and phosphatidylserine exposure, and (iv) greater extents of epinephrine induced apoptosis in lymphocytes, and higher plasma norepinephrine/epinephrine, myeloperoxidase, and interleukin‐6 concentrations than HF patients without lymphocytopenia and normal counterparts did. Therefore, we conclude that increased sympathetic activation and oxidative stress/pro‐inflammatory status may cause lymphocytopenia by activating programmed lymphocyte death in the HF patients. Moreover, a low lymphocyte count correlates with reduced hemodynamics and functional aerobic capacity.