title: Increased neutrophil lifespan in patients with congestive heart failure.
abstract: OBJECTIVE
  Congestive heart failure (CHF) can be thought of as a state of chronic immune activation. Polymorphonuclear neutrophil (PMN) apoptosis is one of the mechanisms responsible for the resolution of inflammation. A reduced PMN apoptotic rate in CHF patients may generate a persistent inflammatory response and hence mediate tissue damage in this group of patients. We aimed to measure levels of spontaneous apoptosis of circulating PMNs in CHF patients and in controls, and to examine whether NYHA class, left ventricular ejection fraction (LV-EF), and laboratory parameters of inflammation, endothelial damage, and of liver and renal function, could predict the rate of PMN apoptosis in CHF patients.
  
  
  RESULTS
  A total of 29 CHF patients and 26 controls were studied. Propidium iodide and flow cytometry were used to assess PMN apoptosis. Delay in PMN apoptosis was expressed as percentage (expressed as median, first and third quartiles) of surviving PMNs in the study subjects. We found an increased percentage of surviving PMNs [38(27.1-47.1)] in CHF patients compared with controls [19.4 (15.8-25.2)] (P < 0.05). The PMN survival rate in the CHF group was correlated to NYHA class, and plasma levels of C-reactive protein and alkaline phosphatase, while it was inversely correlated to LV-EF and protein levels. A positive relationship between PMN survival and increased ex vivo endothelial apoptosis was found.
  
  
  CONCLUSIONS
  Increased PMN lifespan in patients with worsening CHF could be used as a novel measurement of tissue and endothelial damage in this group of patients.
authors.affiliation: Department of Internal Medicine, Research Center of Cardiovascular Biology, University of Genova, Viale Benedetto XV/6, 16132 Genova, Italy.
authors.forename: Irene
authors.initials: I
authors.lastname: Tracchi
authors.forename: Giorgio
authors.initials: G
authors.lastname: Ghigliotti
authors.forename: Marzia
authors.initials: M
authors.lastname: Mura
authors.forename: Silvano
authors.initials: S
authors.lastname: Garibaldi
authors.forename: Paolo
authors.initials: P
authors.lastname: Spallarossa
authors.forename: Chiara
authors.initials: C
authors.lastname: Barisione
authors.forename: Valentina
authors.initials: V
authors.lastname: Boasi
authors.forename: Michele
authors.initials: M
authors.lastname: Brunelli
authors.forename: Luca
authors.initials: L
authors.lastname: Corsiglia
authors.forename: Antonio
authors.initials: A
authors.lastname: Barsotti
authors.forename: Claudio
authors.initials: C
authors.lastname: Brunelli
mesh_terms: D000368:Aged; D017209:Apoptosis / Q000502:physiology*; D002097:C-Reactive Protein / Q000378:metabolism; D002478:Cells, Cultured; D018450:Disease Progression; D004730:Endothelium, Vascular / Q000473:pathology; D004797:Enzyme-Linked Immunosorbent Assay; D005500:Follow-Up Studies; D006333:Heart Failure / Q000097:blood / Q000473:pathology* / Q000503:physiopathology; D006801:Humans; D007958:Leukocyte Count; D009504:Neutrophils / Q000473:pathology*; D011379:Prognosis; D011446:Prospective Studies; D013318:Stroke Volume
chemical_list: D002097:C-Reactive Protein