Rate of telomere shortening and cardiovascular damage: a longitudinal study in the 1946 British Birth Cohort.

Author: Masi S1, D'Aiuto F2, Martin-Ruiz C3, Kahn T4, Wong A5, Ghosh AK5, Whincup P6, Kuh D5, Hughes A7, von Zglinicki T3, Hardy R5, Deanfield JE8; on behalf of the NSHD scientific and data collection teams.
Affiliation:
1Vascular Physiology Unit, Institute of Cardiovascular Science, University College London, London, UK King's College Hospital, NHS Foundation Trust, London, UK. 2Periodontology Unit, Eastman Dental Institute, University College of London, London, UK. 3Institute of Aging and Health, Newcastle University, Newcastle upon Tyne, UK. 4Vascular Physiology Unit, Institute of Cardiovascular Science, University College London, London, UK. 5MRC Unit for Lifelong Health and Ageing, Institute of Epidemiology and Health Care, University College London, London, UK. 6Division of Population Health Sciences and Education, St George's University of London, London, UK. 7National Heart and Lung Institute, Imperial College Academic Health Sciences Centre, London, UK. 8Vascular Physiology Unit, Institute of Cardiovascular Science, University College London, London, UK National Centre for Cardiovascular Prevention and Outcomes, University College London, 170 Tottenham Court Road, W1T 7HA London, UK j.deanfield@ucl.ac.uk.
Conference/Journal: Eur Heart J.
Date published: 2014 Jun 22
Other: Pages: ehu226 , Word Count: 259



AIM:
Cross-sectional studies reported associations between short leucocyte telomere length (LTL) and measures of vascular and cardiac damage. However, the contribution of LTL dynamics to the age-related process of cardiovascular (CV) remodelling remains unknown. In this study, we explored whether the rate of LTL shortening can predict CV phenotypes over 10-year follow-up and the influence of established CV risk factors on this relationship.
METHODS AND RESULTS:
All the participants from the MRC National Survey of Health and Development (NSHD) with measures of LTL and traditional CV risk factors at 53 and 60-64 years and common carotid intima-media thickness (cIMT), cardiac mass and left ventricular function at 60-64 years were included. LTL was measured by real-time polymerase chain reaction and available at both time points in 1033 individuals. While LTL at 53 years was not linked with any CV phenotype at 60-64 years, a negative association was found between LTL and cIMT at 60-64 years (β = -0.017, P = 0.015). However, the strongest association was found between rate of telomere shortening between 53 and 60-64 years and values of cIMT at 60-64 years (β = -0.020, P = 0.006). This association was not affected by adjustment for traditional CV risk factors. Cardiac measurements were not associated with cross-sectional or longitudinal measures of LTL.
CONCLUSION:
These findings suggest that the rate of progression of cellular ageing in late midlife (reflected by the rate of LTL attrition) relates to vascular damage, independently from contribution of CV risk factor exposure.
© The Author 2014. Published by Oxford University Press on behalf of the European Society of Cardiology.
KEYWORDS:
Ageing; Cardiovascular diseases; Carotid artery; Telomeres shortening

PMID: 24957070

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