Artery Research (Feb 2020)

P36 Leukocyte Telomere Length is Inversely Associated with Wave Reflection in 566 Normotensive and Never-treated Hypertensive Subjects

  • Ilkka Pörsti,
  • Milja Honkonen,
  • Kati Vääräniemi,
  • Outi Saijonmaa,
  • Antti Tikkakoski,
  • Jenni Koskela,
  • Arttu Eräranta,
  • Mika Kähönen,
  • Jukka Mustonen,
  • Frej Fyhrquist

DOI
https://doi.org/10.2991/artres.k.191224.068
Journal volume & issue
Vol. 25, no. 1

Abstract

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Background: Telomeres are short segments in chromosome ends, the length of which is reduced during cell life-cycles. We examined the association of leukocyte telomere length and short telomere proportion with hemodynamic variables. Methods: Altogether 566 subjects (279 women and 287 men) without cardiovascular disease and medications with direct cardiovascular influences were subjected supine recordings for 5 minutes. Haemodynamics were captured using continuous tonometric pulse wave analysis and whole-body impedance cardiography. The analyses were adjusted for age, body mass index (BMI), alcohol use, smoking, plasma chemistry, and estimated glomerular filtration rate (eGFR). Results: In univariate analyses, leukocyte telomere length correlated with age, BMI, eGFR, aortic blood pressure, augmentation index, pulse wave velocity, and systemic vascular resistance (p < 0.05 for all). Short telomere proportion correlated with age, BMI, eGFR, aortic systolic blood pressure, augmentation index, and pulse wave velocity (p < 0.05 for all). In linear regression analyses of all hemodynamic variables, leukocyte telomere length was only an independent explanatory factor for augmentation index (Beta −0.006, p = 0.032), while short telomere proportion was not an explanatory factor for any of the hemodynamic variables, in contrast to age, BMI and several cardiovascular risk factors. Conclusion: Augmentation index was predominantly related with chronological aging, but also with leukocyte telomere length, suggesting that this variable of central wave reflection is a moderate marker of vascular biological aging.