title: Leukocyte redistribution: effects of beta blockers in patients with chronic heart failure.
abstract: BACKGROUND
  Overproduction of pro-inflammatory cytokines is a well established factor in the progression of chronic heart failure (CHF). Changes in cellular immunity have not been widely studied, and the impact of standard medication is uncertain. Here we investigate whether a leukocyte redistribution occurs in CHF and whether this effect is influenced by beta-blocker therapy.
  
  
  METHODS
  We prospectively studied 75 patients with systolic CHF (age: 68+/-11 years, left ventricular ejection fraction 32+/-11%, New York Heart Association class 2.5+/-0.7) and 20 age-matched healthy control subjects (age: 63+/-10 years). We measured the response of cells to endotoxin exposure in vitro, analysed subsets of lymphocytes using flow cytometry, and assessed plasma levels of the pro-inflammatory markers interleukin 1, 6, tumor necrosis factor-alpha, and soluble tumor necrosis factor receptors 1 and 2.
  
  
  RESULTS
  While no differences in the number of leukocytes were noted between patients with CHF and healthy controls, we detected relative lymphopenia in patients with CHF (p<0.001 vs. control), mostly driven by reductions in T helper cells and B cells (both p<0.05). The number of neutrophils was increased (p<0.01). These effects were pronounced in patients who were beta-blocker naïve (32% of all patients with CHF). Increased plasma levels of soluble tumor necrosis receptor-1 correlated with the relative number of lymphocyte subsets.
  
  
  CONCLUSIONS
  In patients with CHF, we detected a redistribution of leukocyte subsets, i.e. an increase in neutrophils with relative lymphopenia. These effects were pronounced in patients who were beta-blocker naïve. The underlying mechanism remains to be elucidated.
authors.affiliation: Applied Cachexia Research, Dept. of Cardiology, Charité Medical School, Campus Virchow-Clinic, Berlin, Germany. stephan.von.haehling@web.de
authors.forename: Stephan
authors.initials: S
authors.lastname: von Haehling
authors.forename: Joerg C
authors.initials: JC
authors.lastname: Schefold
authors.forename: Ewa
authors.initials: E
authors.lastname: Jankowska
authors.forename: Wolfram
authors.initials: W
authors.lastname: Doehner
authors.forename: Jochen
authors.initials: J
authors.lastname: Springer
authors.forename: Kristin
authors.initials: K
authors.lastname: Strohschein
authors.forename: Sabine
authors.initials: S
authors.lastname: Genth-Zotz
authors.forename: Hans-Dieter
authors.initials: HD
authors.lastname: Volk
authors.forename: Philip
authors.initials: P
authors.lastname: Poole-Wilson
authors.forename: Stefan D
authors.initials: SD
authors.lastname: Anker
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000494:pharmacology* / Q000627:therapeutic use; D000368:Aged; D016022:Case-Control Studies; D005434:Flow Cytometry; D006333:Heart Failure / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology; D006801:Humans; D007962:Leukocytes / Q000166:cytology*; D008875:Middle Aged; D011446:Prospective Studies; D016277:Ventricular Function, Left
chemical_list: D000319:Adrenergic beta-Antagonists