White Cell Telomere Length and Risk of Premature Myocardial Infarction

TLDR

Biological age, reflected by mean leukocyte telomere length, may differ from chronological age and contribute to age‑related diseases, with shorter telomeres indicating increased biological age. The study examined whether individuals with premature myocardial infarction have shorter leukocyte telomeres. Mean terminal restriction fragment length was compared between 203 premature MI cases (<50 years) and 180 age‑ and sex‑matched controls. Premature MI cases had significantly shorter telomeres (≈300 bp shorter, equivalent to 11.3 years older) independent of other risk factors, and those with shorter telomeres had a 2.8–3.2‑fold higher MI risk, supporting a role for biological age in coronary disease.

Abstract

Objective— Biological age may be distinct from chronological age and contribute to the pathogenesis of age-related diseases. Mean telomeres lengths provide an assessment of biological age with shorter telomeres, indicating increased biological age. We investigated whether subjects with premature myocardial infarction (MI) had shorter leukocyte telomeres. Methods and Results— Mean terminal restriction fragment (TRF) length, a measure of average telomere size, was compared in leukocyte DNA of 203 cases with a premature MI (&lt;50 years) and 180 controls. Age- and sex-adjusted mean TRF length of cases was significantly shorter than that of controls (difference 299.7±69.3 base pairs, P &lt;0.0001) and on average equivalent to controls 11.3 years older. The difference in mean TRF length between cases and controls was not accounted for by other coronary risk factors. Compared with subjects in the highest quartile for telomere length, the risk of myocardial infarction was increased between 2.8- and 3.2-fold ( P &lt;0.0001) in subjects with shorter than average telomeres. Conclusions— The findings support the concept that biological age may play a role in the etiology of coronary heart disease and have potentially important implications for our understanding of its genetic etiology, pathogenesis, and variable age of onset.