title: Telomere length, risk of coronary heart disease, and statin treatment in the West of Scotland Primary Prevention Study: a nested case-control study.
abstract: BACKGROUND
  Inter-individual differences in biological ageing could affect susceptibility to coronary heart disease. Our aim was to determine whether mean leucocyte telomere length is a predictor of the development of coronary heart disease.
  
  
  METHODS
  We compared telomere lengths at recruitment in 484 individuals in the West of Scotland Primary Prevention Study (WOSCOPS) who went on to develop coronary heart disease events with those from 1058 matched controls who remained event free. We also investigated whether there was any association between telomere length and observed clinical benefit of statin treatment in WOSCOPS.
  
  
  RESULTS
  Mean telomere length decreased with age by 9% per decade (95% CI 3.6-14.1; p=0.001) in controls; much the same trend was seen in cases (-5.9% per decade, -3.1 to 14.1; p=0.1902). Individuals in the middle and the lowest tertiles of telomere length were more at risk of developing a coronary heart disease event than were individuals in the highest tertile (odds ratio [OR] for coronary heart disease: 1.51, 95% CI 1.15-1.98; p=0.0029 in the middle tertile; 1.44, 1.10-1.90, p=0.0090 in the lowest). In placebo-treated patients, the risk of coronary heart disease was almost double in those in the lower two tertiles of telomere length compared with those in the highest tertile (1.93, 1.33-2.80, p=0.0005 in the middle tertile; 1.94, 1.33-2.84, p=0.0006 in the lowest). By contrast, in patients treated with pravastatin, the increased risk with shorter telomeres was substantially attenuated (1.12, 0.75-1.69, p=0.5755 in the middle tertile; 1.02, 0.68-1.52, p=0.9380 in the lowest).
  
  
  CONCLUSIONS
  Mean leucocyte telomere length is a predictor of future coronary heart disease events in middle-aged, high-risk men and could identify individuals who would benefit most from statin treatment. Our findings lend support to the hypothesis that differences in biological ageing might contribute to the risk--and variability in age of onset--of coronary heart disease.
authors.affiliation: Department of Cardiovascular Sciences, University of Leicester, Leicester, UK.
authors.forename: Scott W
authors.initials: SW
authors.lastname: Brouilette
authors.forename: Jasbir S
authors.initials: JS
authors.lastname: Moore
authors.forename: Alex D
authors.initials: AD
authors.lastname: McMahon
authors.forename: John R
authors.initials: JR
authors.lastname: Thompson
authors.forename: Ian
authors.initials: I
authors.lastname: Ford
authors.forename: James
authors.initials: J
authors.lastname: Shepherd
authors.forename: Chris J
authors.initials: CJ
authors.lastname: Packard
authors.forename: Nilesh J
authors.initials: NJ
authors.lastname: Samani
mesh_terms: D000375:Aging / Q000502:physiology; D001794:Blood Pressure / Q000187:drug effects; D016022:Case-Control Studies; D002784:Cholesterol / Q000097:blood; D003327:Coronary Disease / Q000209:etiology* / Q000517:prevention & control; D005500:Follow-Up Studies; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D017035:Pravastatin / Q000627:therapeutic use*; D012307:Risk Factors; D012606:Scotland; D016615:Telomere / Q000187:drug effects* / Q000235:genetics / Q000502:physiology
chemical_list: D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D002784:Cholesterol; D017035:Pravastatin