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

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.