title: Leukocyte labile iron pool in patients with systolic heart failure.
abstract: BACKGROUND
  Data regarding sources of oxidative stress in the failing myocardium are sparse. Leukocytes actively participate in the oxidative damage observed in human heart failure (HF). The intracellular labile iron pool (LIP) represents a source of toxic reactive oxygen species.
  
  
  METHODS
  We studied patients with chronic systolic HF who had a left ventricular ejection fraction (LVEF) 45%. We examined the LIP status in different populations of leukocytes in HF patients and we investigated its association with clinical and laboratory parameters, including conventional inflammatory markers.
  
  
  RESULTS
  Sixty patients were finally included in the analysis (mean age: 67 ± 11 years, 54 men, 42 with ischemic cardiomyopathy). The multivariate logistic regression analysis showed that only LIP in granulocytes (OR: 0.73; 95% CI: 0.55-0.98; p=0.039) and right ventricular systolic pressure (RVSP) (OR: 0.95; 95% CI: 0.92-0.99; p=0.027) were independently associated with severe LV systolic dysfunction (LVEF30%). The correlation analysis revealed that LVEF was inversely associated with LIP in granulocytes (Spearman's rho: -0.39, p=0.002), LIP in monocytes (Spearman's rho: -0.35, p=0.007), and RVSP (Spearman's rho: -0.43, p=0.003). No significant correlation between LVEF and inflammatory indexes was noted.
  
  
  CONCLUSIONS
  LIP in granulocytes is independently associated with the severity of LV dysfunction in patients with systolic HF. Intracellular redox active iron may represent a source of leukocyte reactive oxygen species in this setting.
authors.affiliation: Department of Cardiology, University of Ioannina Medical School, Ioannina, Greece. p.korantzopoulos@yahoo.gr
authors.forename: Panagiotis
authors.initials: P
authors.lastname: Korantzopoulos
authors.forename: Chara
authors.initials: C
authors.lastname: Vlachou
authors.forename: Anna
authors.initials: A
authors.lastname: Kotsia
authors.forename: Kallirroi
authors.initials: K
authors.lastname: Kalantzi
authors.forename: Alexandra
authors.initials: A
authors.lastname: Barbouti
authors.forename: Dimitrios
authors.initials: D
authors.lastname: Galaris
authors.forename: John A
authors.initials: JA
authors.lastname: Goudevenos
mesh_terms: D000368:Aged; D005260:Female; D005500:Follow-Up Studies; D054143:Heart Failure, Systolic / Q000378:metabolism* / Q000503:physiopathology; D006801:Humans; D007501:Iron / Q000378:metabolism*; D007962:Leukocytes / Q000378:metabolism*; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D018384:Oxidative Stress; D011379:Prognosis; D017382:Reactive Oxygen Species / Q000378:metabolism; D013318:Stroke Volume; D016277:Ventricular Function, Left / Q000502:physiology*; D017725:Ventricular Pressure
chemical_list: D017382:Reactive Oxygen Species; D007501:Iron