Abstract 13444: Longer Telomere Length is Associated With More Distensible Carotid Arteries in a Healthy Adult Population

Abstract

Introduction: Chronological age is associated with loss of arterial distensibility leading to greater cardiac afterload and inefficient systemic perfusion. It is not known if cellular aging, marked by a loss of telomeres, underlies vascular aging. We thus examined the association of leukocyte telomere length (LTL) with common carotid distensibility (CD) in a healthy adult population. Methods: We analyzed data from 119 adults free of clinical cardiovascular disease (ages 21-80 years, 39% African American, 60% women, from 99 families) with familial history of early onset coronary artery disease (30x coverage, Illumina HiSeq) for both 4 (LTL4) and 7 (LTL7) contiguous telomere motif repeats (TTAGGG or CCCTAA) using the approach of Ding et al (2014). Mean CD of both carotid arteries was calculated from systolic and diastolic carotid diameters measured using B-mode ultrasound and simultaneous measurement of brachial artery pulse pressure (follow-up time 0-5 years from the LTL visit). We used mixed model regression to account for non-independence of data in families. Results: The mean (SD) of LTL4 was 94851 (16370) and of LTL7 was 80666 (15001) repeats. Adjusting for age at LTL measurement, follow-up time to carotid measurement, sex, race, systolic and diastolic blood pressure, LDL- and HDL-cholesterol levels, current smoking and diabetes, 1 SD higher level of LTL4 was associated with 2.0 х 10 -4 (p = 0.027), and 1 SD higher level of LTL7 with 1.8 х 10 -4 mmHg -1 (p = 0.048) higher CD, which is equivalent to CD at a chronological age that is lower by 4.4 and 4.0 years, respectively. Hypertension is not significantly associated with CD (p = 0.49) when added to this model. Conclusions: Greater LTL is associated with more distensible carotid arteries independent of cardiac risk factors including chronological age and blood pressure. Preserved telomere length represents healthy cellular aging in terms of fewer cell divisions, and thus greater vascular reparative reserve, which may lead to preserved arterial distensibility. This mechanism may partly explain the reported association of greater telomere length with lower risk of vascular events including coronary disease, heart failure and stroke.