Activation of Lymphocyte Autophagy/Apoptosis Reflects Hemodynamic Inefficiency and Functional Aerobic Impairment in Patients with Heart Failure

This study investigated whether lymphocytopenia results from activated lymphocyte autophagy/apoptosis, which reflects hemodynamic inefficiency and functional aerobic impairment in the HF patients.One hundred twenty-seven HF patients were divided into three groups: HF with non-(lymphocytes≧2,000 cells/ml, n=45), mild-(1,500 cells/ml≧lymphocytes<2,000 cells/ml, n=39), and severe-(lymphocytes<1,500 cells/ml, n=43) lymphocytopenia groups. Lymphocyte autophagy/apoptosis, ventilatory/hemodynamic efficiencies, and generic/disease-specific quality of life (QoL)were analyzed in these HF patients and 35 normal counterparts.The results demonstrated that HF patients with severe lymphocytopenia revealed (i) more G protein-coupled receptor kinase-2 (GRK-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 concentrationsthan HF patients without lymphocytopenia and normal counterparts did. Moreover, lymphocyte caspase-3 activation was an effect modifier, which modulated the correlation status between lymphocyte count and GRK-2 level.Lymphocyte count was positively correlated with peak cardiac output and VO2peak in patients with HF. Additionally, HF with lymphocytepen...
Source: Clinical Science - Category: Biomedical Science Authors: Source Type: research