title: Telomere length of circulating leukocytes is decreased in patients with chronic heart failure.
abstract: OBJECTIVE
  This study sought to test the hypothesis that patients with chronic heart failure (CHF) have shorter telomeres compared with age-balanced and gender-balanced healthy individuals.
  
  
  BACKGROUND
  Telomere length is considered to be a marker of biological aging. Chronic heart failure might be viewed as a condition associated with accelerated biological aging.
  
  
  METHODS
  The telomere length ratio of leukocytes was determined prospectively by a quantitative polymerase chain reaction-based method in a case-control setting involving 803 participants: 183 healthy individuals and 620 CHF patients, ages 40 to 80 years, New York Heart Association functional class II to IV, and left ventricular ejection fraction of 0.40 or less.
  
  
  RESULTS
  The median telomere length ratio was 0.64 (interquartile range [IQR] 0.47 to 0.88) in CHF patients compared with 1.05 (IQR 0.86 to 1.29) in control patients (p < 0.001). The telomere length ratio in CHF patients related to severity of disease (median value [IQR] of patients with New York Heart Association class II, III, or IV function was 0.67 [0.48 to 0.92], 0.63 [0.46 to 0.86], and 0.55 [0.46 to 0.75], respectively; p for trend <0.05). In addition, telomeres were shorter in patients with an ischemic compared with a nonischemic etiology of CHF. Patients with none, 1 (coronary, cerebral, or peripheral vascular disease), 2 (any combination of the previous), or 3 atherosclerotic manifestations had a median (IQR) telomere length of 0.72 (0.51 to 1.01), 0.65 (0.48 to 0.87), 0.48 (0.39 to 0.72), and 0.43 (0.27 to 0.67), respectively (p for trend <0.001).
  
  
  CONCLUSIONS
  Telomere length is shorter in patients with CHF compared with age-balanced and gender-balanced control patients, and related to the severity of disease. In addition, telomere length was incrementally shorter according to the presence and extent of atherosclerotic disease manifestations.
authors.affiliation: Department of Cardiology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands. p.van.der.harst@thorax.umcg.nl
authors.forename: Pim
authors.initials: P
authors.lastname: van der Harst
authors.forename: Gerrit
authors.initials: G
authors.lastname: van der Steege
authors.forename: Rudolf A
authors.initials: RA
authors.lastname: de Boer
authors.forename: Adriaan A
authors.initials: AA
authors.lastname: Voors
authors.forename: Alistair S
authors.initials: AS
authors.lastname: Hall
authors.forename: Marcel J
authors.initials: MJ
authors.lastname: Mulder
authors.forename: Wiek H
authors.initials: WH
authors.lastname: van Gilst
authors.forename: Dirk J
authors.initials: DJ
authors.lastname: van Veldhuisen
mesh_terms: D000368:Aged; D050197:Atherosclerosis; D016022:Case-Control Studies; D005260:Female; D006333:Heart Failure / Q000209:etiology / Q000235:genetics*; D006801:Humans; D007962:Leukocytes; D008297:Male; D011446:Prospective Studies; D012720:Severity of Illness Index; D016615:Telomere / Q000648:ultrastructure*