%0 Journal Article %J Mech Ageing Dev %D 2012 %T Telomere-associated polymorphisms correlate with cardiovascular disease mortality in Caucasian women: the Cardiovascular Health Study. %A Burnett-Hartman, Andrea N %A Fitzpatrick, Annette L %A Kronmal, Richard A %A Psaty, Bruce M %A Jenny, Nancy S %A Bis, Josh C %A Tracy, Russ P %A Kimura, Masayuki %A Aviv, Abraham %K Aged %K Aged, 80 and over %K Cardiovascular Diseases %K Cohort Studies %K European Continental Ancestry Group %K Female %K Humans %K Leukocytes %K Male %K Polymorphism, Genetic %K Polymorphism, Single Nucleotide %K Risk %K RNA %K Sex Factors %K Telomerase %K Telomere %X

Leukocyte telomere length (LTL) is linked to cardiovascular disease (CVD); however, it is unclear if LTL has an etiologic role in CVD. To gain insight into the LTL and CVD relationship, a cohort study of CVD mortality and single nucleotide polymorphisms (SNPs) in OBFC1 and TERC, genes related to LTL, was conducted among 3271 Caucasian participants ages ≥65 years enrolled 1989-1990 in the Cardiovascular Health Study. Leukocyte DNA was genotyped for SNPs in OBFC1 (rs4387287 and rs9419958) and TERC (rs3772190) that were previously associated with LTL through genome-wide association studies. Cox regression was used to estimate adjusted hazard ratios (HRs) and 95% confidence intervals (CIs). The OBFC1 SNPs were in linkage disequilibrium (r(2)=0.99), and both SNPs were similarly associated with CVD mortality in women. For women, there was a decreased risk of CVD death associated with the minor allele (rs4387287), HR=0.7; 95% CI: 0.5-0.9 (CC vs. AC) and HR=0.5; 95% CI: 0.20-1.4 (CC vs. AA) (P-trend <0.01). For men there was no association, HR=1.0; 95% CI: 0.7-1.3 (CC vs. AC) and HR=1.7; 95% CI: 0.8-3.6 (CC vs. AA) (P-trend=0.64). These findings support the hypothesis that telomere biology and associated genes may play a role in CVD-related death, particularly among women.

%B Mech Ageing Dev %V 133 %P 275-81 %8 2012 May %G eng %N 5 %1 http://www.ncbi.nlm.nih.gov/pubmed/22449406?dopt=Abstract %R 10.1016/j.mad.2012.03.002