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.