Men with short telomeres may have a greater risk for heart disease

Men with short telomeres - repetitive strips of DNA that cap the ends of chromosomes - may have a higher risk of developing coronary heart disease than those with long telomeres, according to an Article in this week's issue of The Lancet.

Telomeres act like an internal biological clock for living organisms because they get shorter every time a cell divides. Shorter telomeres indicate older cells. Previous research has shown that people with coronary heart disease are more likely to have short telomeres, but whether shorter telomere length is a consequence of heart disease or a predictive marker for it, has been unclear until now.

Nilesh Samani (British Heart Foundation and the University of Leicester, UK) and colleagues measured telomere length in white blood cell DNA of men aged 45–64 years already enrolled in the West of Scotland Primary Prevention Study (WOSCOPS). They compared the telomere lengths of 484 men who went on to develop coronary heart disease with those of 1058 men who remained disease free. They found that the men that developed coronary heart disease had shorter telomeres than those that remained disease free.

Because WOSCOPS randomly assigned some patients to receive statin treatment, the researchers also investigated the effect of telomere length on the risk of heart disease in patients on statins versus those on placebo.

They found that in placebo-treated patients, the risk of coronary heart disease was almost double in those with short telomeres when compared with those with relatively long telomeres. By contrast, in patients receiving statin treatment, the risk of heart disease was substantially reduced for those with short telomeres.

Professor Samani concludes: "We have shown that leukocyte [white blood cell] telomere length is associated with future coronary heart disease events in middle-aged, high-risk men, and that it could identify individuals who would benefit most from statin treatment. . . Our findings support the hypothesis that differences in biological ageing might contribute to the risk—and variability in age of onset—of coronary heart disease"