<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Burnett-Hartman AN</submitter><funding>NIA NIH HHS</funding><funding>NIDDK NIH HHS</funding><funding>NCRR NIH HHS</funding><funding>NHLBI NIH HHS</funding><pagination>275-81</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3391009</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>133(5)</volume><pubmed_abstract>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 &lt;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.</pubmed_abstract><journal>Mechanisms of ageing and development</journal><pubmed_title>Telomere-associated polymorphisms correlate with cardiovascular disease mortality in Caucasian women: the Cardiovascular Health Study.</pubmed_title><pmcid>PMC3391009</pmcid><funding_grant_id>N01-HC-85239</funding_grant_id><funding_grant_id>N01-HC-75150</funding_grant_id><funding_grant_id>AG-20098</funding_grant_id><funding_grant_id>R56 AG020098</funding_grant_id><funding_grant_id>N01-HC-85079</funding_grant_id><funding_grant_id>U01 HL080295</funding_grant_id><funding_grant_id>AG-027058</funding_grant_id><funding_grant_id>R56 AG023629</funding_grant_id><funding_grant_id>N01-HC-85080</funding_grant_id><funding_grant_id>R01 AG023629</funding_grant_id><funding_grant_id>N01HC85086</funding_grant_id><funding_grant_id>N01 HC035129</funding_grant_id><funding_grant_id>N01 HC075150</funding_grant_id><funding_grant_id>R01 HL80698-01</funding_grant_id><funding_grant_id>N01-HC-85085</funding_grant_id><funding_grant_id>N01-HC-85086</funding_grant_id><funding_grant_id>M01-RR00425</funding_grant_id><funding_grant_id>N01-HC-85083</funding_grant_id><funding_grant_id>N01-HC-85084</funding_grant_id><funding_grant_id>N01-HC-85081</funding_grant_id><funding_grant_id>N01-HC-85082</funding_grant_id><funding_grant_id>R01 AG020098</funding_grant_id><funding_grant_id>N01HC75150</funding_grant_id><funding_grant_id>R01 AG015928</funding_grant_id><funding_grant_id>N01 HC015103</funding_grant_id><funding_grant_id>N01HC55222</funding_grant_id><funding_grant_id>N01 HC-55222</funding_grant_id><funding_grant_id>M01 RR000425</funding_grant_id><funding_grant_id>N01HC85079</funding_grant_id><funding_grant_id>R01 HL080698</funding_grant_id><funding_grant_id>DK063491</funding_grant_id><funding_grant_id>P30 DK063491</funding_grant_id><funding_grant_id>AG-023629</funding_grant_id><funding_grant_id>N01 HC045133</funding_grant_id><funding_grant_id>R01 AG027058</funding_grant_id><pubmed_authors>Burnett-Hartman AN</pubmed_authors><pubmed_authors>Jenny NS</pubmed_authors><pubmed_authors>Bis JC</pubmed_authors><pubmed_authors>Psaty BM</pubmed_authors><pubmed_authors>Aviv A</pubmed_authors><pubmed_authors>Kronmal RA</pubmed_authors><pubmed_authors>Fitzpatrick AL</pubmed_authors><pubmed_authors>Tracy RP</pubmed_authors><pubmed_authors>Kimura M</pubmed_authors></additional><is_claimable>false</is_claimable><name>Telomere-associated polymorphisms correlate with cardiovascular disease mortality in Caucasian women: the Cardiovascular Health Study.</name><description>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 &lt;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.</description><dates><release>2012-01-01T00:00:00Z</release><publication>2012 May</publication><modification>2021-02-20T19:35:17Z</modification><creation>2019-03-27T00:55:18Z</creation></dates><accession>S-EPMC3391009</accession><cross_references><pubmed>22449406</pubmed><doi>10.1016/j.mad.2012.03.002</doi></cross_references></HashMap>