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Biological ageing and cardiovascular disease
  1. Nilesh J Samani1,
  2. Pim van der Harst2
  1. 1
    Department of Cardiovascular Sciences, University of Leicester, Glenfield Hospital, Leicester, UK
  2. 2
    Department of Cardiology, University Medical Centre Groningen, University of Groningen, The Netherlands
  1. Professor N J Samani, Department of Cardiovascular Sciences, University of Leicester, Clinical Sciences Wing, Glenfield Hospital, Groby Road, Leicester LE3 9QP, UK; njs{at}

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At a population level, several environmental, lifestyle and genetic risk factors contribute to the development of coronary artery disease (CAD) and heart failure. However, at an individual level, both susceptibility to, and the age of onset of, these conditions vary considerably even for subjects with apparently similar risk factor profiles. Any mechanism that is proposed to explain this interindividual variation needs to take into account the age association of these diseases (ie, that they are more common with age) and integrate the impact of known risk factors. Here we discuss emerging evidence that suggests that at least part of the interindividual difference in susceptibility to, and in age of onset of, CAD, and possibly other cardiovascular diseases including heart failure, reflects interindividual variation in biological ageing and that mean telomere length acts as a valuable marker of this process.


Telomeres are the extreme ends of eukaryotic chromosomes. They are made up of a large number of tandem repeats of a simple DNA sequence (in humans TTAGGG). Telomeres are important structures involved in cell cycle control and maintenance of chromosomal stability.1 2 They have three features that mark them as possible markers of interindividual variation in biological ageing:

  • The numbers of repeats (and hence telomere lengths) have a significant genetic determination and vary between individual subjects at birth and through life.36

  • In somatic cells telomeres shorten progressively with repeated cell division.7 This is because DNA polymerase cannot fully replicate the 3′ end of linear DNA during mitosis, the so-called end replication problem (fig 1), and some telomeric DNA is lost during each division.1 2 In utero, in stems cells, and in many cancer cells, the enzyme telomerase helps to maintain the telomere (fig 1) but telomerase is transcriptionally repressed in most somatic cells.1 2 …

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  • Competing interests: None.