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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2006;26:e114.)
© 2006 American Heart Association, Inc.

Atherosclerosis and Lipoproteins

Degenerative Aortic Valve Stenosis, but not Coronary Disease, Is Associated With Shorter Telomere Length in the Elderly

David J. Kurz; Barbara Kloeckener-Gruissem; Alexander Akhmedov; Franz R. Eberli; Ines Bühler; Wolfgang Berger; Osmund Bertel; Thomas F. Lüscher

From CardioVascular Center (D.J.K., F.R.E., I.B., T.F.L.), Cardiology, University Hospital; Cardiovascular Research (D.J.K., A.A., T.F.L.), Institute of Physiology, University of Zurich; Department of Molecular Genetics (B.K.-G., W.B.), Institute of Medical Genetics, University of Zurich; Cardiology (D.J.K., O.B.), Triemli Hospital, Zurich, Switzerland.

Correspondence to David J. Kurz, MD, Cardiovascular Research, Institute of Physiology, University of Zurich-Irchel, Winterthurerstrasse 190, CH-8057 Zurich, Switzerland. E-mail david.kurz{at}hispeed.ch

Objective— The mechanisms responsible for the age-related increase in the incidence of calcific aortic valve stenosis (CAS) are unclear but may include telomere-driven cellular senescence. Because telomere length varies widely among individuals of the same age, we hypothesized that patients with shorter telomeres would be prone to develop CAS late in life.

Methods and Results— Mean telomere length was measured in leukocytes from a cohort of 193 patients 70 years of age with and without CAS. Pilot experiments performed in 30 patients with CAS and controls pair-matched for age, sex, and presence or absence of coronary disease demonstrated significantly shorter telomeres in the CAS group both by Southern blot hybridization (5.75±0.55 kbp versus 6.27±0.7 kbp, P=0.0023) and by a quantitative polymerase chain reaction-based technique (relative telomere length 0.88±0.19 versus 1.0±0.19, P=0.01). This finding was then confirmed in the whole cohort (CAS n=64, controls n=129, relative telomere length=0.86±0.16 versus 0.94±0.12, P=0.0003). Both groups were comparable for potential confounding characteristics. Subgroup analysis according to the presence or absence of coronary disease demonstrated no association of this disorder with telomere length.

Conclusions— In the elderly, calcific aortic stenosis, but not coronary disease, is associated with shorter leukocyte telomere length.

The mechanisms responsible for the age-related increase in the incidence of calcific aortic valve stenosis (CAS) are unclear but may include telomere-driven cellular senescence. Because telomere length varies widely among individuals of the same age, we hypothesized that patients with shorter telomeres would be prone to develop CAS late in life. In the elderly, calcific aortic stenosis, but not coronary disease, is associated with shorter leukocyte telomere length.

Key Words: aging • aortic stenosis • coronary disease • risk factors • telomere

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