title: Prognostic value of leukocyte telomere length in patients with stable coronary artery disease: data from the Heart and Soul Study.
abstract: BACKGROUND
  Telomere shortening has been proposed as a marker of biological aging. Whether leukocyte telomere length is associated with mortality among patients with stable coronary artery disease (CAD) is unknown.
  
  
  RESULTS
  We measured leukocyte telomere length in 780 patients with stable CAD in a prospective cohort study. Participants were categorized by quartiles of telomere length. Hazard Ratios (HRs) and 95% confidence intervals were calculated for all-cause mortality, heart failure (HF) hospitalization, and cardiovascular (CV) events. After 4.4 years of follow-up there were 166 deaths. Compared with participants in the highest telomere length quartile, those in the lowest quartile were at increased risk of death (age-adjusted HR 1.8; 95% CI 1.2 to 2.9). After multivariate adjustment for clinical (HR 2.1; CI 1.3 to 3.3), inflammatory (HR 2.0; CI 1.2 to 3.2), and echocardiographic (HR 1.9; CI 1.0 to 3.5) risk factors, patients in the lowest quartile of telomere length remained at significantly increased risk of death compared to those in the highest quartile. Patients in the lowest quartile of telomere length were also at significantly increased risk of HF hospitalization (HR 2.6; CI 1.1 to 6.0) but not CV events (HR 1.7; CI 0.9 to 3.5).
  
  
  CONCLUSIONS
  Reduced leukocyte telomere length is associated with all-cause mortality in patients with stable CAD. The prognostic value of short telomeres in predicting death is not completely captured by existing clinical, inflammatory, and echocardiographic markers of risk.
authors.affiliation: Department of Medicine, Box 0124, University of California San Francisco, CA 94143-0124, USA. rfarzanehfar@medicine.ucsf.edu
authors.forename: Ramin
authors.initials: R
authors.lastname: Farzaneh-Far
authors.forename: Richard M
authors.initials: RM
authors.lastname: Cawthon
authors.forename: Beeya
authors.initials: B
authors.lastname: Na
authors.forename: Warren S
authors.initials: WS
authors.lastname: Browner
authors.forename: Nelson B
authors.initials: NB
authors.lastname: Schiller
authors.forename: Mary A
authors.initials: MA
authors.lastname: Whooley
mesh_terms: D000368:Aged; D002097:C-Reactive Protein / Q000378:metabolism; D002318:Cardiovascular Diseases / Q000235:genetics* / Q000276:immunology / Q000401:mortality; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging / Q000235:genetics* / Q000401:mortality / Q000473:pathology; D005260:Female; D005500:Follow-Up Studies; D006333:Heart Failure / Q000235:genetics* / Q000276:immunology / Q000401:mortality; D006760:Hospitalization; D006801:Humans; D053208:Kaplan-Meier Estimate; D007962:Leukocytes / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D011379:Prognosis; D011446:Prospective Studies; D018570:Risk Assessment; D012495:San Francisco / Q000453:epidemiology; D016615:Telomere / Q000648:ultrastructure*; D013997:Time Factors; D014463:Ultrasonography
chemical_list: D002097:C-Reactive Protein