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Biological ageing and cardiovascular disease

¹ Department of Cardiovascular Sciences, University of Leicester, Glenfield Hospital, Leicester, UK
² Department of Cardiology, University Medical Centre Groningen, University of Groningen, The Netherlands

Correspondence to:
Professor N J Samani, Department of Cardiovascular Sciences, University of Leicester, Clinical Sciences Wing, Glenfield Hospital, Groby Road, Leicester LE3 9QP, UK; njs@le.ac.uk

The first 150 words of the full text of this article appear below.

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

 
Telomeres are the extreme ends of eukaryotic chromosomes. They are made . . . [Full text of this article]