Dataset Information

Association of shorter mean telomere length with risk of incident myocardial infarction: a prospective, nested case-control approach.

ABSTRACT:

Background

Recent data have implicated telomere length shortening as a potential risk predictor for cardiovascular disease. However, to date, prospective epidemiological data are scarce.

Methods

Using leukocyte DNA samples collected at baseline in a prospective cohort of 14,916 initially healthy American men, we examined the relationship of mean telomere repeat copy number to single gene copy number (T/S ratio), using a re-modified quantitative polymerase chain reaction protocol, among 337 white males who subsequently developed an incident myocardial infarction (MI), and among an equal number of age- and smoking-matched white males who remained free of reported vascular disease during follow-up (controls).

Results

The mean follow-up time since randomization was 3.85 y. The T/S ratio was inversely correlated with age in the controls (R=-0.114; p=0.036). The log(e)-transformed T/S ratios were significantly smaller in the MI cases (3.41+/-0.63) than the MI controls (3.52+/-0.78) (p=0.01). In a multi-variable adjusted analysis, decreased T/S ratio was significantly associated with risk of MI (odds ratio=1.621; 95%CI=1.140-2.304; p=0.007).

Conclusions

The present investigation has shown an association of telomere length shortening with increased risk of incident myocardial infarction, further suggesting the importance of telomere biology in atherogenesis.

SUBMITTER: Zee RY

PROVIDER: S-EPMC2752372 | biostudies-literature | 2009 May

REPOSITORIES: biostudies-literature

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Publications

Association of shorter mean telomere length with risk of incident myocardial infarction: a prospective, nested case-control approach.

Zee Robert Y L RY Michaud Sherri E SE Germer Soren S Ridker Paul M PM

Clinica chimica acta; international journal of clinical chemistry 20090213 1-2

<h4>Background</h4>Recent data have implicated telomere length shortening as a potential risk predictor for cardiovascular disease. However, to date, prospective epidemiological data are scarce.<h4>Methods</h4>Using leukocyte DNA samples collected at baseline in a prospective cohort of 14,916 initially healthy American men, we examined the relationship of mean telomere repeat copy number to single gene copy number (T/S ratio), using a re-modified quantitative polymerase chain reaction protocol, ...[more]

PMID: 19217888

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Project description:BackgroundFrailty is a multidimensional syndrome of decline that affects multiple systems and predisposes to adverse health outcomes. Although chronological age is the major risk factor, inter-individual variation in risk is not fully understood. Leucocyte telomere length (LTL), a proposed marker of biological age, has been associated with risk of many diseases. We sought to determine whether LTL is associated with risk of frailty.MethodsWe utilized cross-sectional data from 441 781 UK Biobank participants (aged 40-69 years), with complete data on frailty indicators and LTL. Frailty was defined as the presence of at least three of five indicators: weaker grip strength, slower walking pace, weight loss in the past year, lower physical activity, and exhaustion in the past 2 weeks. LTL was measured using a validated qPCR method and reported as a ratio of the telomere repeat number (T) to a single-copy gene (S) (T/S ratio). Association of LTL with frailty was evaluated using adjusted (chronological age, sex, deprivation, smoking, alcohol intake, body mass index, and multimorbidity) multinomial and ordinal regression models, and results are presented as relative risk (RRR) or odds ratios (OR), respectively, alongside the 95% confidence interval (CI). Mendelian randomization (MR), using 131 genetic variants associated with LTL, was used to assess if the association of LTL with frailty was causal.ResultsFrail participants (4.6%) were older (median age difference (95% CI): 3 (2.5; 3.5) years, P = 2.73 × 10-33 ), more likely to be female (61%, P = 1.97 × 10-129 ), and had shorter LTL (-0.13SD vs. 0.03SD, P = 5.43 × 10-111 ) than non-frail. In adjusted analyses, both age and LTL were associated with frailty (RRR = 1.03 (95% CI: 1.02; 1.04) per year of older chronological age, P = 3.99 × 10-12 ; 1.10 (1.08; 1.11) per SD shorter LTL, P = 1.46 × 10-30 ). Within each age group (40-49, 50-59, 60-69 years), the prevalence of frailty was about 33% higher in participants with shorter (-2SD) versus longer telomeres (+2SD). MR analysis showed an association of LTL with frailty that was directionally consistent with the observational association, but not statistically significant (MR-Median: OR (95% CI): 1.08 (0.98; 1.19) per SD shorter LTL, P = 0.13).ConclusionsInter-individual variation in LTL is associated with the risk of frailty independently of chronological age and other risk factors. Our findings provide evidence for an additional biological determinant of frailty.

Dataset Information

Association of shorter mean telomere length with risk of incident myocardial infarction: a prospective, nested case-control approach.

Background

Methods

Results

Conclusions

Publications

Association of shorter mean telomere length with risk of incident myocardial infarction: a prospective, nested case-control approach.

Similar Datasets

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